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La prevalencia de la hipertensión arterial en la población gene-

ral del Perú fue de 23,7%, en mayores de 18 años, lo que co-

rrespondería a 3 650 000 habitantes, estimado en base al censo

2005, con un predominio de hipertensos varones de 13,4% so-

bre hipertensas mujeres de 10,3%. Predominio de sexo mascu-

lino que persiste en los hipertensos de la costa, sierra y selva. La prevalencia de la hipertensión arterial por sexo, de toda la

población, fue 27,1% en varones y 20,4% en mujeres

# data[].attributes.attachment_link.authors[].name
Colegio Médico del Perú, CMP, Lima, Perú

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View of Epidemiology of Arterial Hypertension in Peru

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Return to Article Details Epidemiology of Arterial Hypertension in Peru

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http://scielo.sld.cu/scielo.php?script=sci_arttext&pid=S1029-30192016001100015
Aunque todavía no se conocen las causas específicas que provocan la hipertensión arterial, sí se ha relacionado con una serie de factores que suelen estar presentes en la mayoría de las personas que la sufren, tales como: dieta con alto contenido de sal, grasa o colesterol, además de las condiciones crónicas (problemas renales y hormonales, diabetes mellitus y colesterol alto), antecedentes familiares de la enfermedad, falta de actividad física, vejez (mientras mayor sea la persona existe más probabilidad de padecerla), sobrepeso, obesidad, color de la piel, algunos medicamentos anticonceptivos, estrés y consumo excesivo de tabaco o alcohol.

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Se describe como factores de riesgo la obesidad, predisposición genética, nefropatías. Este artículo menciona la presencia de la enfermedad en niños, siendo esta perteneciente a la clasificación como secundaria. Evalúa los factores que llevan a que las cifras en niños se incrementen y las posibles explicaciones como factores de riesgo.

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Según un estudio de cohorte prospectiva realizado a 277 000 individuos de 40 a 69 años, se observó que el estilo de vida poco saludable y la susceptibilidad genética a la Presión Arterial se asociaron con niveles más altos de Presión Arterial y además un mayor riesgo de incidentes posteriores de ECV

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Affiliations

¹ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.).

² MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.).

³ Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

⁴ William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁵ National Institute for Health Research, Barts Cardiovascular Biomedical Research Center, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁶ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.) p.elliott@imperial.ac.uk itzoulak@cc.uoi.gr.

Free article

Free article

Affiliations

¹ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.).

² MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.).

³ Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

⁴ William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁵ National Institute for Health Research, Barts Cardiovascular Biomedical Research Center, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁶ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.) p.elliott@imperial.ac.uk itzoulak@cc.uoi.gr.

Abstract

Background: High blood pressure (BP) is a major risk factor for cardiovascular diseases (CVDs), the leading cause of mortality worldwide. Both heritable and lifestyle risk factors contribute to elevated BP levels. We aimed to investigate the extent to which lifestyle factors could offset the effect of an adverse BP genetic profile and its effect on CVD risk.

Methods: We constructed a genetic risk score for high BP by using 314 published BP loci in 277 005 individuals without previous CVD from the UK Biobank study, a prospective cohort of individuals aged 40 to 69 years, with a median of 6.11 years of follow-up. We scored participants according to their lifestyle factors including body mass index, healthy diet, sedentary lifestyle, alcohol consumption, smoking, and urinary sodium excretion levels measured at recruitment. We examined the association between tertiles of genetic risk and tertiles of lifestyle score with BP levels and incident CVD by using linear regression and Cox regression models, respectively.

Results: Healthy lifestyle score was strongly associated with BP ( P<10⁻³²⁰) for systolic and diastolic BP and CVD events regardless of the underlying BP genetic risk. Participants with a favorable in comparison with an unfavorable lifestyle (bottom versus top tertile lifestyle score) had 3.6, 3.5, and 3.6 mm Hg lower systolic BP in low, middle, and high genetic risk groups, respectively ( P for interaction=0.0006). Similarly, favorable in comparison with unfavorable lifestyle showed 30%, 33%, and 31% lower risk of CVD among participants in low, middle, and high genetic risk groups, respectively ( P for interaction=0.99).

Conclusions: Our data further support population-wide efforts to lower BP in the population via lifestyle modification. The advantages and disadvantages of disclosing genetic predisposition to high BP for risk stratification needs careful evaluation.

Keywords: blood pressure; cardiovascular diseases; genetic predisposition to disease; genetics; healthy lifestyle; risk.

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national center for biotechnology information

# data[].attributes.attachment_link.title
Genetic Predisposition to High Blood Pressure and Lifestyle Factors: Associations With Midlife Blood Pressure Levels and Cardiovascular Events - PubMed

# data[].attributes.attachment_link.description
1 Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.). 2 MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.). 3 Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

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PREVALENCIA E INCIDENCIA DE

HIPERTENSIÓN ARTERIAL EN PERÚ: REVISIÓN

SISTEMÁTICA Y METAANÁLISIS
Los hallazgos muestran que uno de cada cinco peruanos tiene hipertensión, y que aparecen cuatro nuevos casos por 100 personas en un año, además solo la mitad de los pacientes hipertensos

tienen el diagnóstico previo de su condición.

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La hipertensión arterial (HTA) es la primera causa de muerte y discapacidad a nivel mundial. Uno de cada 3 adultos en España es hipertenso (66% en los > 60 años). A pesar de la mejora en el manejo de la hipertensión con el tiempo, solo la mitad de los pacientes hipertensos tratados están adecuadamente controlados. Esto se traduce en 40.000 muertes cardiovasculares anuales atribuibles al H T. Entre los determinantes modificables del descontrol de la presión arterial (PA) en España se encuentran: a) el fenómeno de bata blanca (responsable del 20-50% del falso descontrol) por no uso de monitorización ambulatoria de la PA (uso actual, 20 %) o automedición de la PA (uso, 60 %) para confirmar el diagnóstico de HTA; b) adherencia insuficiente de los pacientes a estilos de vida reductores de la PA (p. ej., solo el 40% de los pacientes hipertensos tienen una ingesta de sodio < 2,4 g/día, o siguen un consejo de reducción de peso), y c) uso de monoterapia farmacológica (≈50%). suele ser insuficiente para lograr un control adecuado.

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doi: 10.1016/S1889-1837(18)30066-7.

Affiliations

¹ Departamento de Medicina Preventiva y Salud Pública, Universidad Autónoma de Madrid/IdiPAZ-CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, España.

² Departamento de Medicina Preventiva y Salud Pública, Universidad Autónoma de Madrid/IdiPAZ-CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, España. Electronic address: joseramon.banegas@uam.es.

doi: 10.1016/S1889-1837(18)30066-7.

Affiliations

¹ Departamento de Medicina Preventiva y Salud Pública, Universidad Autónoma de Madrid/IdiPAZ-CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, España.

² Departamento de Medicina Preventiva y Salud Pública, Universidad Autónoma de Madrid/IdiPAZ-CIBER de Epidemiología y Salud Pública (CIBERESP), Madrid, España. Electronic address: joseramon.banegas@uam.es.

Abstract

Hypertension (HT) is the first cause of death and disability worldwide. One in 3 adults in Spain is hypertensive (66% in those > 60 years). Despite improvement in hypertension management over time, only half of treated hypertensive patients are adequately controlled. This translates in 40,000 annual cardiovascular deaths attributable to H T. Among modifable determinants of lack of blood pressure (BP) control in Spain are: a) the white coat phenomenon (accounting for 20-50% of false lack of control) due to not using ambulatory BP monitoring (current use, 20%) or self-BP measurement (use, 60%) for confirming HT diagnosis; b) insufficient patients adherence to BP reducing lifestyles (e.g., only 40% of hypertensive patients have a sodium intake < 2.4 g/day, or follow a weight reduction advice), and c) use of drug monotherapy (≈50%), usually insufficient to achieve adequate control. © 2017 SEHLELHA. Published by Elsevier España, S.L.U. All rights reserved.

Keywords: Ambulatory blood pressure monitoring; Automedida de la presión arterial; Hipertensión arterial; Hypertension; Monitorización ambulatoria de la presión arterial; Self-blood pressure measurement.

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[Ambulatory blood pressure monitoring is a useful tool for all patients].

de la Sierra A. de la Sierra A. Hipertens Riesgo Vasc. 2017 Jan-Mar;34(1):45-49. doi: 10.1016/j.hipert.2016.06.004. Epub 2016 Jul 26. Hipertens Riesgo Vasc. 2017. PMID: 27474527 Review. Spanish.

Prognosis of Masked and White Coat Uncontrolled Hypertension Detected by Ambulatory Blood Pressure Monitoring in Elderly Treated Hypertensive Patients.

Pierdomenico SD, Pierdomenico AM, Coccina F, Porreca E. Pierdomenico SD, et al. Am J Hypertens. 2017 Nov 1;30(11):1106-1111. doi: 10.1093/ajh/hpx104. Am J Hypertens. 2017. PMID: 29059303

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antihypertensive agents / therapeutic use

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.description
Hypertension (HT) is the first cause of death and disability worldwide. One in 3 adults in Spain is hypertensive (66% in those > 60 years). Despite improvement in hypertension management over time, only half of treated hypertensive patients are adequately controlled. This translates in 40,000 ann ...

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http://www.scielo.org.pe/pdf/afm/v81n1/1025-5583-afm-81-01-00033.pdf
Según el presente estudio, en Perú se ha reportado que la HTA fue mayor en el sexo masculino en comparación al sexo femenino. Entre los factores asociados que aumentaron la probabilidad de HTA fueron la edad, sobrepeso y obesidad para hombres y mujeres, mientras que ser del resto de la costa, sierra y selva disminuyeron la probabilidad.

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En un estudio transversal se tuvo como resultado que la PAD (presión arterial diastólica) y la PAM (presión arterial media)ajustadas fueron menores en los fumadores actuales frente a los no fumadores y la PAS (presión arterial sistólica) ajustada fue menor en los fumadores actuales frente a los exfumadores (P < 0,05). Además, el PP (presión de pulso) ajustado tiende a disminuir de manera constante a medida que aumentan los paquetes-año en los fumadores actuales. Los hallazgos revelaron que las presiones arteriales ajustadas fueron menores en fumadores actuales versus no fumadores y exfumadores. No se observó ningún efecto dependiente de la dosis significativo del tabaquismo actual sobre los índices de presión arterial, excepto la PP. Dejar de fumar se asoció significativamente con un mayor riesgo de hipertensión. Sin embargo, el tabaquismo actual no era un factor de riesgo de hipertensión.

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doi: 10.1186/s12889-017-4802-x.

Affiliations

¹ Qingdao Women and Children's Hospital, Qingdao University, Qingdao, Shandong, 266011, China.

² Inner Mongolia Center for Disease Control and Prevention, Hohhot, China.

³ National Office for Maternal and Child Health Surveillance of China, Department of Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, China.

⁴ China-Japan Friendship Hospital, Beijing, China.

⁵ Fangshan District Center for Disease Control and Prevention, Beijing, China.

⁶ Department of Epidemiology and Statistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.

⁷ Department of Epidemiology and Statistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China. guangliang_shan@163.com.

Free PMC article

Guoju Li et al. BMC Public Health.

Free PMC article

doi: 10.1186/s12889-017-4802-x.

Affiliations

¹ Qingdao Women and Children's Hospital, Qingdao University, Qingdao, Shandong, 266011, China.

² Inner Mongolia Center for Disease Control and Prevention, Hohhot, China.

³ National Office for Maternal and Child Health Surveillance of China, Department of Obstetrics, Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, West China Second University Hospital, Sichuan University, Chengdu, China.

⁴ China-Japan Friendship Hospital, Beijing, China.

⁵ Fangshan District Center for Disease Control and Prevention, Beijing, China.

⁶ Department of Epidemiology and Statistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.

⁷ Department of Epidemiology and Statistics, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China. guangliang_shan@163.com.

Abstract

Background: Cigarette smoking is a known risk factor for cardiovascular disease (CVD), but the association between smoking and blood pressure is unclear. Thus, the current study examined the association between cigarette smoking and blood pressure in men.

Methods: Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial pressure (MAP) and pulse pressure (PP) were examined using digital blood pressure measuring device, and smoking status was determined with China National Health Survey.

Results: The ANCOVA showed that the adjusted DBP and MAP were lower in current smokers versus nonsmokers and the adjusted SBP was lower in current smokers versus former smokers (P < 0.05). Additionally, the adjusted PP tend to be decreased steadily as the pack·years increased in current smokers. In a fully adjusted logistic regression model, former smokers had increased ORs (95% CI) of 1.48 (1.01, 2.18) of hypertension and current smokers had not increased ORs (95% CI) of 0.83 (0.61, 1.12), compared with never smokers.

Conclusions: The findings revealed that the adjusted blood pressure were lower in current smokers versus nonsmokers and former smokers. No significant dose-dependent effect of current smoking on blood pressure indices except PP was observed. Smoking cessation was significantly associated with an increased risk of hypertension. However, current smoking was not a risk factor of hypertension.

Keywords: Blood pressure; Hypertension; Smoking; Tobacco.

Conflict of interest statement

Ethics approval and consent to participate

The study was approved by the Ethics Committee of the Institute of Basic Medical Sciences of the Chinese Academy of Medical Sciences (028-2013), and all participants written informed consent. The study was performed in accordance with approved national guidelines.

Consent for publication

All authors made significant contributions to the manuscript and all authors have read and approved the final version as well as agreed with the publishment on BMC Public Health.

Competing interests

The authors declared that they have no competing interests.

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

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References

Chow CK, Teo KK, Rangarajan S, Islam S, Gupta R, Avezum A, Bahonar A, Chifamba J, Dagenais G, Diaz R, et al. Prevalence, awareness, treatment, and control of hypertension in rural and urban communities in high-, middle-, and low-income countries. JAMA. 2013;310(9):959-968. doi: 10.1001/jama.2013.184182. - DOI - PubMed

Li W, Gu H, Teo KK, Bo J, Wang Y, Yang J, Wang X, Zhang H, Sun Y, Jia X, et al. Hypertension prevalence, awareness, treatment, and control in 115 rural and urban communities involving 47 000 people from China. J Hypertens. 2016;34(1):39-46. doi: 10.1097/HJH.0000000000000745. - DOI - PubMed

Lim SS, Vos T, Flaxman AD, Danaei G, Shibuya K, Adair-Rohani H, Amann M, Anderson HR, Andrews KG, Aryee M, et al. A comparative risk assessment of burden of disease and injury attributable to 67 risk factors and risk factor clusters in 21 regions, 1990-2010: a systematic analysis for the Global Burden of Disease Study 2010. Lancet. 2012;380(9859):2224-2260. doi: 10.1016/S0140-6736(12)61766-8. - DOI - PMC - PubMed

WHO . A Global Brief on Hypertension: Silent Killer, Global Public Health Crisis; World Health Day 2013. Geneva: WHO; 2013. pp. 1-39.

Vasily V. Smoking prevalence and attributable disease burden in 195 countries and territories, 1990-2015: a systematic analysis from the Global Burden of Disease Study 2015. 2017. - PMC - PubMed

# data[].attributes.attachment_link.keywords[]
smoking cessation / statistics & numerical data*

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
The association between smoking and blood pressure in men: a cross-sectional study - PubMed

# data[].attributes.attachment_link.description
The findings revealed that the adjusted blood pressure were lower in current smokers versus nonsmokers and former smokers. No significant dose-dependent effect of current smoking on blood pressure indices except PP was observed. Smoking cessation was significantly associated with an increased risk o ...

# data[].attributes.body
Mayor riesgo de hipertensión arterial en personas con estilo de vida poco saludable y con predisposición genética. https://pubmed.ncbi.nlm.nih.gov/29254930/

# data[].attributes.attachment_link.readable_text
Affiliations

¹ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.).

² MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.).

³ Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

⁴ William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁵ National Institute for Health Research, Barts Cardiovascular Biomedical Research Center, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁶ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.) p.elliott@imperial.ac.uk itzoulak@cc.uoi.gr.

Free article

Free article

Affiliations

¹ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.).

² MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.).

³ Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

⁴ William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁵ National Institute for Health Research, Barts Cardiovascular Biomedical Research Center, Queen Mary University of London, United Kingdom (H.W., M.C.).

⁶ Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.) p.elliott@imperial.ac.uk itzoulak@cc.uoi.gr.

Abstract

Background: High blood pressure (BP) is a major risk factor for cardiovascular diseases (CVDs), the leading cause of mortality worldwide. Both heritable and lifestyle risk factors contribute to elevated BP levels. We aimed to investigate the extent to which lifestyle factors could offset the effect of an adverse BP genetic profile and its effect on CVD risk.

Methods: We constructed a genetic risk score for high BP by using 314 published BP loci in 277 005 individuals without previous CVD from the UK Biobank study, a prospective cohort of individuals aged 40 to 69 years, with a median of 6.11 years of follow-up. We scored participants according to their lifestyle factors including body mass index, healthy diet, sedentary lifestyle, alcohol consumption, smoking, and urinary sodium excretion levels measured at recruitment. We examined the association between tertiles of genetic risk and tertiles of lifestyle score with BP levels and incident CVD by using linear regression and Cox regression models, respectively.

Results: Healthy lifestyle score was strongly associated with BP ( P<10⁻³²⁰) for systolic and diastolic BP and CVD events regardless of the underlying BP genetic risk. Participants with a favorable in comparison with an unfavorable lifestyle (bottom versus top tertile lifestyle score) had 3.6, 3.5, and 3.6 mm Hg lower systolic BP in low, middle, and high genetic risk groups, respectively ( P for interaction=0.0006). Similarly, favorable in comparison with unfavorable lifestyle showed 30%, 33%, and 31% lower risk of CVD among participants in low, middle, and high genetic risk groups, respectively ( P for interaction=0.99).

Conclusions: Our data further support population-wide efforts to lower BP in the population via lifestyle modification. The advantages and disadvantages of disclosing genetic predisposition to high BP for risk stratification needs careful evaluation.

Keywords: blood pressure; cardiovascular diseases; genetic predisposition to disease; genetics; healthy lifestyle; risk.

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The effect of socioeconomic deprivation on the association between an extended measurement of unhealthy lifestyle factors and health outcomes: a prospective analysis of the UK Biobank cohort.

Foster HME, Celis-Morales CA, Nicholl BI, Petermann-Rocha F, Pell JP, Gill JMR, O'Donnell CA, Mair FS. Foster HME, et al. Lancet Public Health. 2018 Dec;3(12):e576-e585. doi: 10.1016/S2468-2667(18)30200-7. Epub 2018 Nov 20. Lancet Public Health. 2018. PMID: 30467019

Blood Pressure and Risk of Cardiovascular Disease in UK Biobank: A Mendelian Randomization Study.

Wan EYF, Fung WT, Schooling CM, Au Yeung SL, Kwok MK, Yu EYT, Wang Y, Chan EWY, Wong ICK, Lam CLK. Wan EYF, et al. Hypertension. 2021 Feb;77(2):367-375. doi: 10.1161/HYPERTENSIONAHA.120.16138. Epub 2021 Jan 4. Hypertension. 2021. PMID: 33390054

Ultra-processed food intake is associated with grip strength decline in middle-aged and older adults: a prospective analysis of the TCLSIH study.

Zhang S, Gu Y, Rayamajhi S, Thapa A, Meng G, Zhang Q, Liu L, Wu H, Zhang T, Wang X, Dong J, Zheng X, Cao Z, Zhang X, Dong X, Sun S, Wang X, Zhou M, Jia Q, Song K, Huang J, Huo J, Zhang B, Ding G, Qi L, Niu K. Zhang S, et al. Eur J Nutr. 2021 Nov 17. doi: 10.1007/s00394-021-02737-3. Online ahead of print. Eur J Nutr. 2021. PMID: 34791509

# data[].attributes.attachment_link.keywords[]
national center for biotechnology information

# data[].attributes.attachment_link.title
Genetic Predisposition to High Blood Pressure and Lifestyle Factors: Associations With Midlife Blood Pressure Levels and Cardiovascular Events - PubMed

# data[].attributes.attachment_link.description
1 Department of Biostatistics and Epidemiology, School of Public Health, Imperial College London, United Kingdom (R.P., A.D., E.E., H.G., P.E., I.T.). 2 MRC-PHE Centre for Environment, School of Public Health, Imperial College London, United Kingdom (A.D., H.G., P.E., I.T.). 3 Department of Hygiene and Epidemiology, University of Ioannina Medical School, Greece (E.E., I.T.).

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Factores etiológicos de la hipertensión arterial esencial Se han descrito los siguientes factores hipertensinogénicos
1. Obesidad.
2. Resistencia a la insulina.
3. Ingesta elevada de alcohol.
4. Ingesta elevada de sal en pacientes sensibles a la sal.
5. Edad y Sexo.
6. Sedentarismo.
7. Estrés.
8. Ingesta baja de potasio.
9. Ingesta baja de calcio.

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La hipertensión es una patología que se define como un asesino silencioso ya que presenta características asintomáticas,  pero que ocasiona lesiones de forma silente en el corazón, vasos sanguíneos, riñones y cerebro, siempre y cuando no se detecte ni se trate.
Uno de los síntomas más frecuentes es la cefalea, que sobre todo se observa en la hipertensión arterial severa. Otras manifestaciones pueden ser: vértigos, palpitaciones y fatiga.

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Vista de Factores de riesgo y manifestaciones clínicas de la hipertensión arterial | Revista Científica Arbitrada en Investigaciones de la Salud GESTAR. ISSN: 2737-6273.

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FACTORES DE RIESGO:
Según un estudio realizado en Chile, el factor que presenta mayor riesgo para el desarrollo de HTA es la edad (> 25 años), seguido de factores de riesgo modificables, como sobrepeso y obesidad, obesidad abdominal , consumo de sal y DMT2

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1. Zhang Q, Mahapatra T, Huang F, Tang W, Guo Y, Tang S, et al. Association between Anthropometric Measures and Indicators for Hypertension Control among Kazakh-Chinese Hypertension Patients in Xinjiang, China: Results from a Cross-sectional Study. PLoS One 2017; 12 (1): e0170959. [ Links ]

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Factores de riesgo asociados al desarrollo de hipertensión arterial en Chile

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Referencias 1. Zhang Q, Mahapatra T, Huang F, Tang W, Guo Y, Tang S, et al. Association between Anthropometric Measures and Indicators for Hypertension Control among Kazakh-Chinese Hypertension Patients in Xinjiang, China: Results from a Cross-sectional Study. PLoS One 2017; 12 (1): e0170959. [ Links ] 2.

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Factores de Riesgo HTA (Anghela Rodríguez Saavedra)

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Factores de Riesgo HTA (Anghela Rodríguez Saavedra)

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Los factores de riesgo asociados a la hipertensión arterial son la obesidad, la hipercolesterolemia, la edad, el sobrepeso, las concentraciones bajas de HDL y el estilo de vida inadecuado. Las intervenciones para controlar la hipertensión arterial es conseguir la máxima reducción en el riesgo total a largo plazo de la morbilidad y mortalidad cardiovascular, este proceso se debe basar en la prevención primaria y la detección temprana de todos los factores de riesgos reversibles identificados y el manejo adecuado de las condiciones clínicas asociadas como el propio aumento de la tensión arterial.

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http://castellanacardio.es/wp-content/uploads/2010/11/hipertension-arterial-I.pdf#page=19
Autor: Bellido C. et all
Año: 2003
País: España
En este documento nos hace mención que en la etiología se encuentra: el historial familiar, la obesidad, la resistencia a la insulina, la ingesta elevada de alcohol, la ingesta elevada de sal en pacientes sensibles a la sal, la edad, el sexo, el sedentarismo, el estrés, la ingesta baja de potasio y la ingesta baja de calcio.

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https://www.camjol.info/index.php/RCEUCS/article/view/9761

-Un estudio de casos y controles del año 2019 tuvo por objetivo identificar los factores de riesgo asociados a hipertensión arterial en estudiantes de la Universidad Nacional Autónoma de Honduras en el Valle de Sula (UNAH-VS) en el II y III trimestre del 2018 y dentro de los resultados se obtuvo que los factores de riesgo con una importante asociación a la enfermedad son el antecedente familiar de hipertensión familiar en primer grado, la obesidad, el sedentarismo, la dieta no saludable, la hipertrigliceridemia y la hipercolesterolemia y concluye que dentro de los factores de riesgo no modificables, el antecedente familiar de la enfermedad fue el más importante y en los factores de riesgo modificables predominaron aquellos asociados fuertemente a riesgo cardiovascular.

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DOI:
https://doi.org/10.5377/rceucs.v6i2.9761

Palabras clave:
Dislipidemias, Hipertensión, Obesidad.

Resumen

La hipertensión arterial causa millones de fallecimientos anualmente. Su origen es heterogéneo; implicando factores, tanto modificables como no modificables. Objetivos Identificar los factores de riesgo asociados a hipertensión arterial en estudiantes de la Universidad Nacional Autónoma de Honduras en el Valle de Sula (UNAH-VS) en el II y III trimestre del 2018. Pacientes y métodos Se realizó un estudio cuantitativo de casos y controles con una proporción 1:1 durante el II y III trimestre del año 2018 en el Área de Salud de la Subdi- rección de Desarrollo Estudiantil, Cultura, Arte y Deporte (SUDECAD) de la UNAH-VS. Mediante un muestreo no probabilístico por conveniencia, se obtuvo una muestra de 34 universitarios, casos, diagnosticados con hipertensión arterial y 34 controles que no padecían la enfermedad. Resultados 24 (35.29%) de los pacientes eran hombres. Los factores con una importante asociación a la enfermedad son el antecedente familiar de hipertensión familiar en primer grado (OR: 3.8 IC: 95%, 1.3 - 11.2), la obesidad (OR: 5.1 IC: 95%, 1.6 - 16.5), el sedentarismo (OR: 4.8 IC: 95%, 1.6 - 14.2), la dieta no saludable (OR: 7.6 IC: 95%, 1.5 - 37.8), la hipertrigliceridemia (OR: 5.2 IC: 95%, 1.7 - 15.9) y la hipercolesterolemia (OR: 7.3 IC: 95%, 2.2 - 23.5). Conclusiones En los fac- tores de riesgo no modificables, el antecedente familiar de la enfermedad fue el más importante. En los factores de riesgo modificables, predominaron aquellos asociados fuertemente a riesgo cardiovascular.

Biografía del autor/a

Cinea Mabeth Abujieres Galeano, Universidad Nacional Autónoma de Honduras

Médico General Universidad Nacional Autónoma de Honduras en el Valle de Sula.

Kenny Abner Garmendia Robles, Universidad Nacional Autónoma de Honduras

Médico General Universidad Nacional Autónoma de Honduras en el Valle de Sula.

Luis Enrique Figueroa Luna, Universidad Nacional Autónoma de Honduras

Médico General Universidad Nacional Autónoma de Honduras en el Valle de Sula.

Héctor Alejandro Paz Banegas, Universidad Nacional Autónoma de Honduras

Médico General Universidad Nacional Autónoma de Honduras en el Valle de Sula.

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FACTORES DE RIESGO ASOCIADOS A HIPERTENSIÓN ARTERIAL EN ESTUDIANTES

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https://doi.org/10.5377/rceucs.v6i2.9761 Dislipidemias, Hipertensión, Obesidad. La hipertensión arterial causa millones de fallecimientos anualmente. Su origen es heterogéneo; implicando factores, tanto modificables como no modificables. Objetivos Identificar los factores de riesgo asociados a hipertensión arterial en estudiantes de la Universidad Nacional Autónoma de Honduras en el Valle de Sula (UNAH-VS) en el II y III trimestre del 2018.

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https://www.elsevier.es/es-revista-offarm-4-articulo-etiologia-riesgos-hipertension-13021228#:~:text=La%20HTA%20puede%20ser%20debida,neurog%C3%A9nica%20y%20pendiente%20de%20renina.
La HTA puede ser debida a diversas causas y multitud de factores se han relacionado con la patogenia y agravamiento de la hipertensión. A la hora de clasificar la HTA desde un punto de vista etiológico, a grandes rasgos se puede hablar de HTA renal, endocrina, genética, neurogénica y pendiente de renina.

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La hipertensión es una patología crónica no curable que debe ser sometida a tratamiento de por vida y que es susceptible de provocar alteraciones a medio y largo plazo en función del paciente.

La hipertensión arterial (HTA) constituye el principal riesgo de enfermedad cardiovascular y, por tanto, es una de las principales causas de morbilidad y mortalidad cardiovascular causando graves problemas en la expectativa de vida y en su calidad.

La prevalencia de la HTA varía de forma considerable entre las distintas poblaciones según factores sociales, ambientales y genéticos, pero en general su prevalencia oscila entre el 10 y el 20%. En España, la HTA ocupa el primer lugar en la lista de patologías crónicas en cuanto a motivo de consulta en atención primaria, afectando aproximadamente a un 20% de la población.

No hay una definición clara del concepto de HTA, pero de una forma simple se puede definir como un aumento de la presión arterial por encima de los valores considerados como normales. La definición de hipertensión ha estado influida históricamente por la percepción clínica de la relación entre la presión sanguínea y los efectos derivados que afectan a diferentes órganos del cuerpo humano.

El mayor problema radica en la inexistencia de una clara línea divisoria en los límites de presión arterial que permitan diferenciar individuos normotensos de hipertensos y de cuáles son los valores que deben considerarse factores de riesgo.

En 1984, el Comité Americano para el Control, Evaluación y Tratamiento de la HTA (NJC) propuso una nueva clasificación que es la que se utiliza con mayor frecuencia en la actualidad. Ésta considera normales los valores de presión diastólica inferiores a 85 mmHg, mientras que los comprendidos entre 85 y 90 mmHg también son considerados normales, pero ya son indicativos de alarma.

Los datos señalados con anterioridad se refieren a población normal, pero los valores considerados como normales o patológicos pueden variar en función de diversos estados fisiológicos. La hipertensión gestacional o preeclampsia se caracteriza por un aumento en la presión sistólica mayor o igual a 30 mmHg, y de 15 mmHg en la diastólica con respecto a los valores normales de la paciente antes del embarazo. El hallazgo aislado de un valor elevado de la presión arterial no es indicativo de hipertensión, sino que implica la necesidad de encontrar valores elevados de forma repetida, excepto en el caso de una urgencia hipertensiva.

Clasificación de la hipertensión

La clasificación se puede hacer atendiendo a varios criterios: según el valor de la presión arterial, según el grado de repercusión visceral, según la etiología y según el grado de actividad de renina plasmática.

Según el valor de la presión arterial

Hipertensión arterial diastólica. Leve: 90-104 mmHg; moderada: 105-114 mmHg, y grave: superior a 115 mmHg.

Hipertensión arterial sistólica. Superior a 160 mmHg.

Según el grado de repercusión visceral (OMS, 1978)

Fase I. No aparecen signos objetivos de afectación orgánica.

Fase II. Aparecen uno o más de los siguientes signos: hipertrofia del ventrículo izquierdo, arterias de la retina con estrechez focal o generalizada, proteinuria y/o aumento de la concentración de creatinina en plasma.

Fase III. Se producen los siguientes signos clínicos en diferentes órganos: corazón (insuficiencia ventricular izquierda y a veces angina de pecho e infarto de miocardio), cerebro (hemorragia cerebral, trombosis y encefalopatía hipertensiva), fondo del ojo (hemorragias y exudados retinianos), riñón (insuficiencia renal) y vasos (aneurisma disecante).

Según la etiología

Hipertensión arterial esencial. Cuando no existen causas fisiológicas de origen conocido.

Hipertensión secundaria. Se debe a una gran variedad de causas. Se trata de una manifestación de otra patología. Según la enfermedad, los mecanismos que contribuyen a la patogenia de la HTA varían desde efectos hormonales sobre la musculatura lisa vascular a cambios en la hemodinámica. En la mayoría de los casos la hipertensión secundaria se debe a enfermedades renales o tiene su origen en trastornos endocrinometabólicos con alteración en la producción de hormonas como la estimulante del tiroides, tiroideas, aldosterona, glucocorticoides o mineralocorticoides.

Según el grado de actividad de renina plasmática

HTA con actividad de renina plasmástica baja.

HTA con actividad de renina plasmática normal.

HTA con actividad de renina plasmática elevada.

Patogenia de la hipertensión

La HTA puede ser debida a diversas causas y multitud de factores se han relacionado con la patogenia y agravamiento de la hipertensión. A la hora de clasificar la HTA desde un punto de vista etiológico, a grandes rasgos se puede hablar de HTA renal, endocrina, genética, neurogénica y pendiente de renina.

Hipertensión renal

Las alteraciones en la hemodinámica intrarrenal contribuyen a la patogenia de la HTA, y cualquier oclusión en las arterias renales produce un aumento en la presión arterial. La nefroesclerosis, la glomerulonefritis, la nefropatía diabética, infartos renales, trombosis renales, tumores, etc. pueden provocar HTA.

Otro mecanismo por el cual la enfermedad renal posee un papel en la patogenia de la hipertensión está relacionado con la capacidad que tiene el riñón para excretar sal y agua. Un aumento en la retención de sodio y líquidos produce un incremento de la presión arterial.

Hipertensión endocrina

La aldosterona provoca HTA como consecuencia de un aumento en la retención de sodio. Esta hormona es secretada por la zona glomerular de la corteza suprarrenal, y en el aldosteronismo primario la velocidad de secreción aumenta y se vuelve autónoma. La hipertensión resultante es consecuencia del aumento en la retención de sodio y en el volumen plasmático.

Los esteroides también poseen un efecto mineralocorticoide, por lo que en el síndrome de Cushing es característica la HTA. También la hiperplasia renal congénita se acompaña de un exceso de mineralocorticoides e hipertensión.

Hipertensión genética

Los sujetos procedentes de progenitores con HTA padecen la enfermedad con mayor frecuencia que aquellos cuyos padres no la padecieron, demostrándose que la hipertensión puede tener una base genética. En la actualidad ya es un hecho, constatado mediante estudios epidemiológicos, que existe una mayor incidencia de la HTA en familiares de sujetos con la patología establecida, fenómeno denominado como "agrupación familiar".

Hipertensión neurogénica

En las regiones laterales y posteriores del hipotálamo hay centros presores que producen aumentos agudos de la presión arterial, por lo que la lesión cerebral de estructuras que controlan la actividad simpática puede inducir HTA crónica.

El sistema nervioso constituye el mecanismo de control más rápido de la presión. Un aumento de la actividad nerviosa simpática modifica la liberación de renina y de aldosterona, alterando la capacidad renal para excretar sodio y agua, al mismo tiempo que provoca vasoconstricción arteriolar.

Hipertensión dependiente de renina

El sistema renina-angiotensina-aldosterona puede participar en la patogenia de la HTA. La angiotensina II se forma a partir de la angiotensina I por acción de la enzima de conversión de la angiotensina (ECA), siendo un potente vasoconstrictor. Además, la ECA inhibe la formación de cininas, que actúan como sustancias vasodilatadoras.

Riesgos derivados de la HTA

Mortalidad

La importancia que la hipertensión tiene sobre la mortalidad por problemas cardiovasculares es difícil de valorar. Mediante estudios epidemiológicos se observó una relación directa entre hipertensión y mortalidad, incrementándose el riesgo a medida que lo hace la hipertensión. Si se valora el índice de mortalidad por accidentes vasculares cerebrales, cuyo principal desencadenante es la HTA, se llega a idénticas conclusiones. Cuanto antes aparece la HTA menor es la expectativa de vida.

Enfermedad cardiovascular

No cabe duda de que la HTA está reconocida como el mayor factor de riesgo en todo tipo de patologías cardiovasculares, incluida la insuficiencia cardíaca, la cardiopatía isquémica y las enfermedades periféricas vasculares. La incidencia de infarto de miocardio y de enfermedad coronaria es mucho mayor en la población hipertensa que en la normotensa, por lo que la HTA constituye una de las principales causas de muerte cardíaca.

El estudio de la función ventricular izquierda del enfermo hipertenso es de gran interés para estimar el pronóstico evolutivo de la HTA y valorar la terapia a emplear. El sistema cardiovascular se debe adaptar a la sobrecarga funcional, pudiendo aparecer:

Insuficencia cardíaca. La HTA aguda puede ocasionar insuficiencia cardíaca global debido a una sobrecarga mecánica que hace que el corazón sea incapaz de responder a las necesidades metabólicas del organismo. Aparece palidez, disnea, ortopnea, ritmo de galope, sudación, tercer o cuarto tono, cirrosis y distensión en las venas del cuello. En respuesta al aumento de la poscarga, el organismo debe adaptarse a la situación hipertensiva mediante una serie de pasos compensatorios como el aumento de la tasa de filtración glomerular y diuresis, el aumento de la presión de perfusión coronaria y del flujo a través de las arterias, o la reducción en el tono simpático.

Insuficiencia miocárdica sistólica y diastólica. Se altera la cinética del calcio intracelular, con un incremento en las concentraciones de este ión en el interior de las mitocondrias que puede provocar insuficiencia miocárdica sistólica debida a alteraciones en el inotropismo. La disminución de la concentración de calcio en el exterior de las células por desplazamiento anormal hacia el interior de las mitocondrias produce una mayor relajación ventricular que lleva a una insuficiencia miocárdica diastólica.

Arteriolitis. El sistema vascular está compuesto de pequeñas arterias que poseen elasticidad y capacidad contráctil, siendo capaces de regular el tono circulatorio. Durante el estado de hipertensión sostenida las arterias sufren cambios en su distensibilidad, que depende mucho de su calibre.

El aumento de la presión arterial provoca anomalías en la contractibilidad de la musculatura vascular, originando zonas de sobredistensión que provocan turbulencias lesivas sobre la pared. Se produce degeneración de la pared arteriolar, necrosis tisular y estenosis luminal progresiva.

Cuando la HTA es leve, se produce un depósito de material hialino que difunde a las distintas capas del vaso, y con el paso del tiempo tiende a formar colágeno, lo que lleva a la arteriosclerosis hialina. En caso de tratarse de HTA grave las lesiones dependen mucho del calibre del vaso, pero en general son de mayor importancia. Debido a la respuesta adaptativa al incremento de la presión arterial, se produce una cicatrización de los depósitos de fibrinioides que emigran hacia la íntima por fenestraciones de la lámina interna, produciéndose un engrosamiento concéntrico de los vasos con depósitos hialinos focales; es lo que se conoce como arteriolitis hiperplásica.

En el riñón, la HTA produce nefroangiosclerosis. En los estadios iniciales coexisten glomérulos normales con lesionados. Éstos muestran aspecto isquémico con engrosamiento de las paredes capilares. Los glomérulos isquémicos se contraen de forma progresiva y la cápsula de Bowman sufre un depósito de colágeno intracapsular en su cara interna. A medida que la lesión progresa se convierte en nefrosclerosis maligna y aparecen hemorragias capsulares, se forman gotas lipídicas y los glomérulos muestran separaciones entre el endotelio y la membrana basal, con depósitos de fibrina. Se acompaña de un cuadro de hematuria, proteinuria e insuficiencia renal, pudiendo llegar a la anuria.

Globo ocular

Aparecen una serie de lesiones oculares relacionadas con el grado de hipertensión. Se produce un estrechamiento generalizado de las arteriolas. En principio aparece un brillo de las arteriolas, que sufren una ligera depresión marcando las partes del estrechamiento. Cada vez sufren una depresión más clara y se habla de arteriolas en hilo de cobre. Cuando ya es muy avanzada aparecen cambios en el trayecto de las venas, que se denominan "en hilo de plata".

El aumento de la presión arterial provoca anomalías en la contractibilidad de la musculatura vascular, originando zonas de sobredistensión que provocan turbulencias lesivas sobre la pared

Pueden presentarse hemorragias y exudados que se clasifican en función del número de cuadrantes que afectan. Cuando la hipertensión es de predominio diastólico se produce una vasoconstricción segmentaria, disminuyendo el calibre arteriolar y perdiéndose la relación arteria/vena; con el tiempo aparecen lesiones como hemorragias, accidentes vasculares e infiltrados de lípidos. Cuando fracasa la perfusión retiniana se necrotiza la arteriola terminal.

Una de las mayores complicaciones de la HTA son los accidentes cerebrovasculares. El aumento de la presión arterial puede provocar hemorragias cerebrales y, en presencia de aterosclerosis, trombosis. También son frecuentes las encefalopatías hipertensivas, que es un síndrome neurológico caracterizado por cefaleas, somnolencia, vértigo, confusión y, en último termino, convulsiones y un estado de coma.

Entre los accidentes cerebrovasculares destacan los siguientes:

Hemorragias subaracnoideas. Se produce una rotura del aneurisma que provoca cefalea intensa, rigidez de la nuca y ausencia de signos neurológicos focales.

Hemorragias intraparenquimatosas. Ocasiona una intensa cefalea, náuseas, vómitos y defectos sensoriales. Las alteraciones neurológicas dependen de la localización, siendo las talámicas las que presentan un pronóstico más complicado, mientras que las pontianas producen cuadriparesia y un coma profundo.

Factores que alteran la HTA

Una vez establecido el diagnóstico de hipertensión, se debe llevar a cabo un tratamiento no farmacológico y aplicarlo a todos los sujetos, con independencia de que éste pueda ser suficiente o sea necesario añadir una terapia farmacológica. Dicho tratamiento se basa en reducir el consumo de ciertas sustancias y modificar algunos hábitos de vida.

Peso corporal

La HTA desciende con la pérdida de peso derivada de la restricción calórica mediante dietas con bajo contenido en grasas. Asimismo, se recomienda aumentar el consumo de fibras y disminuir el de alimentos de origen animal. Con ello se reducen los niveles de colesterol total y aumenta la fracción HDL; pero estos pacientes vuelven a los niveles previos de HTA tan pronto como abandonan el régimen y recuperan el peso perdido.

Existe una relación entre hipertensión y obesidad, siendo ésta un factor predictivo de la HTA, aunque sobre ambos factores influye el componente genético. Por eso, la reducción del sobrepeso en ocasiones es suficiente para controlar la HTA, y además se evita la sobrecarga del corazón y la aparición de diabetes e hiperlipemia.

Para lograr una mayor efectividad es aconsejable que una dieta pobre en calorías se acompañe de ejercicio físico que, además de ayudar a controlar el peso, produce una disminución de la resistencia vascular periférica.

Una de las mayores incógnitas es la relación real existente entre el consumo de sal y los niveles de HTA. Uno de los datos más curiosos surge en países o zonas con un consumo de sal muy bajo o casi nulo, donde se ha observado que los habitantes raramente padecen hipertensión; pero a medida que éstos emigran a sociedades industrializadas, la incidencia de hipertensión aumenta igual que lo hace el consumo de sal. En la actualidad hay diversos estudios que demuestran la relación cuantitativa directa entre el consumo de sal y la HTA. En países con dietas bajas en sodio es poco frecuente la hipertensión, mientras que en países con gran consumo de sal la incidencia es mayor.

No hay duda de la conveniencia de limitar el consumo de sal en todos los sujetos hipertensos, pero hay que tener en cuenta que el 40% de éstos son lo que podríamos llamar "salrresistentes", por lo que esta medida no modifica los niveles de presión sanguínea.

Sin embargo, en los demás casos la reducción de la ingesta de sodio es a veces ya suficiente para controlar la HTA sin necesidad de recurrir a tratamientos farmacológicos. Hay que recordar que la reducción no debe ser drástica, ya que se pueden producir depleciones salinas que pueden favorecer la hipotensión ortostática.

El sujeto hipertenso no debe consumir más de 5 g al día de sal, reduciendo ésta como condimento de cocina y no consumiendo aquellos alimentos que ya son ricos en sal.

Un sujeto hipertenso no debe sobrepasar los 300 mg de cafeína por día (aproximadamente unas 3 tazas). La cafeína es un excitante que produce taquicardia y un aumento en la resistencia vascular cerebral, siendo capaz de elevar la presión arterial sistólica de forma transitoria, aunque carezca de efectos a largo plazo o sobre la prevalencia de la HTA en la población.

En general, parece aconsejable limitar el consumo de alcohol a los 30 g diarios y no sobrepasar los 80. Se cree que el consumo excesivo de alcohol aumenta la HTA y altera la eficacia de las medidas terapéuticas aplicadas, aunque no existe acuerdo general sobre esta relación cuando el consumo es moderado, e incluso parece que puede resultar beneficioso para el flujo coronario.

Se ha encontrado una correlación positiva entre el consumo de alcohol y la aparición de hemorragias cerebrales que están ligadas a hipertensión, pero, por otra parte, la relación es inversa cuando se relaciona el alcohol con la frecuencia de cardiopatías trombóticas.

No ha podido comprobarse una relación directa entre el consumo de tabaco y la elevación de la presión sanguínea, aunque sí se ha establecido con el riesgo de padecer enfermedad cardiovascular, por lo que el tabaco también debe ser tomado en consideración.

Aunque en algunos casos la población fumadora tiene unos valores de HTA inferiores a los de la no fumadora, este hecho probablemente se debe a una reducción del peso corporal, parámetro que incide directamente en la presión sanguínea. En cualquier caso, las innumerables repercusiones cardiovasculares desfavorables hacen recomendable reducir o suprimir el consumo de tabaco.

El tabaco, además, disminuye la eficacia de algunos fármacos antihipertensivos, aumenta el colesterol total y los triglicéridos y afecta de forma negativa a la circulación sanguínea y a la hemostasia.

Existe una relación entre hipertensión y obesidad, siendo ésta un factor predictivo de la HTA, aunque
sobre ambos factores influye el componente genético

Estilo de vida

Los problemas psicológicos y el estrés favorecen la hipertensión, por lo cual se debe intentar llevar una vida relajada. Por otra parte, el sedentarismo facilita la obesidad, que es uno de los principales factores de riesgo en el desarrollo de la hipertensión, mientras que el ejercicio físico practicado de forma habitual y moderada ayuda a controlar el peso corporal y favorece la relajación.

Medidas dietéticas

Se sugiere que puede haber una correlación inversa entre la ingesta de potasio y la HTA. El exceso de sodio produce menos efectos sobre la presión si éste se administra con potasio, debido a que aumenta la excreción de sodio por el riñón. Algunos investigadores también consideran que el calcio puede afectar a la presión arterial, pero hay datos que apoyan distintas teorías y es difícil extraer conclusiones. Si se confirma su influencia, sería recomendable tenerlo en consideración, sobre todo al analizar la dureza de las aguas. *

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Etiología y riesgos de la hipertensión | Offarm

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La hipertensión es una patología crónica no curable que debe ser sometida a tratamiento de por vida y que es susceptible de provocar alteraciones a medio y largo plazo en función del paciente.

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https://pubmed.ncbi.nlm.nih.gov/15108434/

El objetivo de este articulo es estudiar la prevalencia de hipertensión arterial (HA) en una muestra de población joven de Smolensk, factores de riesgo de HA, conciencia de los pacientes sobre su enfermedad, cumplimiento del tratamiento.

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Abstract

Aim: To study prevalence of arterial hypertension (AH) in young Smolensk population sample, AH risk factors, awareness of the patients about their disease, treatment compliance.

Material and methods: The in-office study covered 1068 employees. In diagnosis of AH, the patient answered the questions about AH risk factors, attitude to treatment.

Results: All was highly prevalent in the examined population (27.9%). Patients under 45 years of age accounted for 38.9% of all the examinees with AH. The risk factors included overweight and obesity (65.5%), smoking (53.5%), family AH history (52.6%). In spite of high awareness about AH (72.4%) and opinion about AH as an important social problem, young patients demonstrate low treatment compliance (12%). This is explained by psychological features of such patients.

Conclusion: It is necessary to examine quality of life of AH patients aged under 45 years, setting up of special schools to maintain educational activity, psychological and rehabilitation care.

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antihypertensive agents / therapeutic use

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national center for biotechnology information

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[Epidemiologic and social aspects of arterial hypertension in subjects of young age (according to the data of examination of organized groups of employees in Smolensk] - PubMed

# data[].attributes.attachment_link.description
Aim: To study prevalence of arterial hypertension (AH) in young Smolensk population sample, AH risk factors, awareness of the patients about their disease, treatment compliance. Material and methods: The in-office study covered 1068 employees. In diagnosis of AH, the patient answered the questions about AH risk factors, attitude to treatment.

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FACTORES DE RIESGO :
-Obesidad
-Índice de masa corporal
-Alto consumo calórico
Antecedente familiar

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Entre los diversos factores de riesgo para las enfermedades cardiovasculares (ECV), la hipertensión arterial (HTA) es considerada uno de los más importantes a nivel mundial, asociándose a eventos coronarios y cerebrovasculares en aproximadamente 60 y 77% de los casos, respectivamente . De igual forma, se estima que para el año 2030 la cifra de afectados por esta enfermedad ascienda en un 8%. Una tendencia similar se ha observado en Ecuador durante la última década, con un ascenso en la incidencia de 256 a 1084 casos por cada 100 mil habitantes durante el periodo 2000-2009 ; asimismo, un reporte previo ha determinado que específicamente en la ciudad de Cuenca, Ecuador la prevalencia de HTA se sitúa en un 25,8% .

Considerando el origen de la HTA como primario (causa desconocida) y secundario a otros trastornos que condicionan la elevación de la presión arterial (PA) , el análisis e identificación de potenciales factores de riesgo ha llevado al estudio de numerosas variables, que pueden influir en la aparición y control de cifras de PA elevadas que tengan importantes implicaciones clínicas, entre las que figuran: edad, raza, tabaquismo, antecedente familiar, menopausia, hábitos nutricionales, obesidad, entre muchos otros ,. El manejo integral de la HTA debe abarcar tanto medidas farmacológicas como no farmacológicas, además, en numerosas oportunidades nos encontramos con pacientes hipertensos que presentan un conjunto de comorbilidades que deben, de igual manera, tratarse simultáneamente ; por ende, la correcta evaluación de este numeroso grupo de sujetos debe incluir la identificación de esos factores ambientales acompañantes.

Ante la importancia epidemiológica que representa la HTA, así como la necesidad de identificar sus principales determinantes, el objetivo del estudio fue determinar los factores de riesgo para HTA en una población de adultos de la ciudad de Cuenca, Ecuador.

DISEÑO Y POBLACIÓN DE ESTUDIO

Se realizó un estudio transversal analítico en la región urbana de Cuenca, la cual está dividida en 16 parroquias: San Sebastián, Bellavista, El Batán, Yanuncay, Sucre, Huayna Capac, Gil Ramírez Dávalos, Sagrario, San Blas, El Vecino, Cañaribamba, Totoracocha, Monay, Machangara, y Hermano Miguel, con una población total de 329 928 habitantes (se sumó a estos un grupo de 1960 individuos que habitan parroquias rurales en el límite con las parroquias urbanas) para un total de 331 888 habitantes, los población mayor de 18 años que habita el área urbana de la ciudad de cuenca fue de 223 798 individuos, para estas estimaciones fueron utilizadas las valoraciones demográficas obtenidas del censo 2010 realizado por el Instituto Nacional de Estadísticas y Censos (INEC).

El cálculo del tamaño de la muestra para cada parroquia se realizó de forma proporcional, mediante un muestreo aleatorio multietápico por conglomerados, donde cada conglomerado estuvo representado por cada una de las 16 parroquias, obteniéndose un tamaño muestral de 318 individuos mayores de 18 años. El criterio de inclusión fue todos los habitantes mayores de 18 años. Dentro de los criterios de exclusión se consideraron a las mujeres en periodo de gestación, individuos recluidos en instituciones penales, hospitales, o cuarteles militares.

Se llevó a cabo un muestreo aleatorio multietápico por conglomerados durante el periodo octubre 2013 a febrero 2014, donde cada uno de los conglomerados estuvo representado por manzanas y a su vez por viviendas las cuales se escogieron al azar manejando la información del censo de la ciudad de cuenca. La tasa de respuesta de los participantes fue de un 98%, donde los sujetos no participantes indicaron no desear participar en el estudio por negarse a ser sometidos a exámenes clínicos o antropométricos; por lo tanto, se realizó un sobremuestreo hasta completar los casos contemplados en la muestra determinada.

EVALUACIÓN DE LOS INDIVIDUOS

A todos los individuos que participaron en el estudio se les realizó historia clínica completa evaluándose la presencia de antecedentes personales de HTA o diabetes mellitus tipo 2 (DM2). El grupo étnico se evaluó fenotípicamente clasificando a los individuos como mestizo, blanco y otros (negro, mulato, montubio). Se evaluó el estatus socioeconómico mediante la escala de Graffar modificado por Méndez-Castellano que estratifica a los sujetos en cinco estratos: clase alta (estrato I); clase media alta, (estrato II); clase media (estrato III), clase obrera (estrato IV), y extrema pobreza (estrato V).

HÁBITOS PSICOBIOLÓGICOS

Se interrogó el consumo de alcohol como autorreporte según la historia clínica en consumidor y no consumidor . Por otra parte, fue evaluado el hábito tabáquico, categorizándose a los individuos en no fumadores, fumadores, y exfumadores a aquellos con un año o más sin consumir ningún tipo de tabaco .

EVALUACIÓN DE ACTIVIDAD FÍSICA

Se realizó el cuestionario internacional de actividad física, el cual fue diseñado para la medición de la actividad física en cuatro dominios: trabajo, transporte, actividades del hogar (jardinería y otros) y ocio (tiempo libre, recreación o ejercicio) . El formato largo del IPAQ (IPAQ-LF) contiene preguntas correspondientes a la frecuencia y duración de la caminata (actividad leve), actividades moderadas o actividad vigorosas de por lo menos 10 min de duración. Los minutos/ semanas de actividad leve, moderada o vigorosa son convertidos a sus equivalentes metabólicos (MET), para así determinar el consumo energético. Los datos se calcularon de acuerdo al resultado MET promedio en cada actividad y a partir de estas consideraciones se realizó el Scoring IPAQ para determinar los patrones de actividad física que son reportados como: actividad física alta, moderada o baja ; dentro de los análisis del IPAQ fueron excluidos ocho individuos, ya que no cumplieron con los criterios de depuración del IPAQ durante los análisis de determinación del patrón de actividad física a través del Scoring IPAQ. Además, se analizó la actividad física expresada en MET/min/sem para el dominio de actividad física de ocio del IPAQ, el cual ha demostrado tener un papel como factor protector cardiovascular , para los análisis del estudio "actividad física de ocio" fue reclasificada en terciles obteniéndose la siguiente clasificación: mujeres (ninguna: 0 MET/min/sem; leve: <33 MET/min/sem; moderada: 33-346,49; alta: ≥346,5 MET/min/sem); hombres (ninguna: 0 MET/min/sem; leve: <66; MET/min/sem; moderada: 66-1046,61; Alta: ≥1046,62 MET/min/sem).

EVALUACIÓN ANTROPOMÉTRICA

Se determinó el peso y la talla de los individuos mediante el uso de balanza-tallímetro Health o Meter Professional (USA) con capacidad 180 kg, para lo cual cada sujeto fue evaluado de pie, en posición erguida, sin calzado ni vestimenta. Los individuos se clasificaron ponderalmente mediante los puntos de corte del índice de masa corporal (IMC) sugeridos por la OMS . La circunferencia abdominal se midió con una cinta métrica metálica Rosscraft, USA, calibrada en milímetros y centímetros, a la altura de la línea media axilar en el punto imaginario que se encuentra entre la parte inferior de la última costilla y el punto más alto de la cresta iliaca, de posición de pie, al final de una espiración .

EVALUACIÓN NUTRICIONAL

Para la evaluación nutricional se aplicó el recordatorio de 24 h, el cual recogió datos de la ingesta de alimentos el día anterior tanto en el desayuno, almuerzo, cena y sus respectivas meriendas, los cuales fueron analizados por un equipo nutricionista para la determinación del consumo diario de calorías (kcal/día). Las calorías consumidas fueron reclasificadas en terciles: tercil 1: <1960,94 kcal/día; tercil 2: 1960,94-2471,93 kcal/día; tercil 3: ≥2471,94 kcal/día.

EVALUACIÓN DE LA PRESIÓN ARTERIAL

La determinación de la presión arterial fue realizada por un equipo de ocho médicos especialistas en medicina familiar y con capacitación para realizar la adecuada técnica de medición por el método auscultatorio, para lo que se utilizó un esfigmomanómetro calibrado y validado. Se le midió al paciente sentado y quieto por lo menos 15 min con los pies en el suelo y el brazo a la altura del corazón, siendo la presión arterial sistólica el punto en el que se escuchó el primero de dos o más sonidos (fase 1) y la presión arterial diastólica es el punto en el que desapareció el sonido (fase 5). Se verificó la PA por tres ocasiones (luego de 10 min de descanso) y se realizó un promedio de las tomas. El diagnóstico de HTA se realizó de dos formas: a) autorreporte como antecedente personal; y b) diagnóstico durante la evaluación clínica, calificándose acorde con los criterios del Comité Norteamericano para la Prevención, Detección, Evaluación y Tratamiento de la HTA en su VII informe (JNC-7) en dos ocasiones separadas .

ANÁLISIS DE LABORATORIO

Se recogieron muestras de sangre (en tubos Vacutainer sin anticoagulante) después de 10 h de ayuno, el suero se obtuvo por centrifugación. Se determinaron los niveles de triglicéridos (TAG), colesterol HDL, colesterol LDL y glucosa plasmática mediante el equipo Mindray b 88, semiaulant. Para la determinación de glicemia, colesterol total, triglicéridos, colesterol LDL se utilizó un kit enzimático-colorimétrico de (Reaactlab); para la cuantificación de colesterol HDL se utilizó un kit enzimático-colorimétrico comercial (Human Frisonex).

VARIABLES METABÓLICAS Y OBESIDAD

Las variables metabólicas y la obesidad abdominal se definieron de acuerdo a los criterios sugeridos por el consenso realizado por la IDF/AHA/NHLBI/WHF/IAS/ IASO (2009) . Según la circunferencia abdominal la obesidad fue clasificada en ≥90 cm para hombres y ≥80 cm para mujeres. TAG elevado: ≥150 mg/dL; colesterol HDL bajo: hombres <40 mg/dL, mujeres <50 mg/dL; glicemia elevada: ≥100 mg/dL, o el uso de medicamentos para el control de alguna alteración respectiva.

ANÁLISIS ESTADÍSTICO

Las variables cualitativas fueron presentadas como frecuencias absolutas y relativas; la prueba Z se utilizó para comparar las proporciones entre grupos y la prueba de chi cuadrado para determinar la asociación entre variables cualitativas. Para evaluar la distribución normal de las variables cuantitativas se utilizó la prueba de Kolmogorov Smirnov. Las variables con distribución normal fueron expresadas con la media ± desviación estándar. Se realizó un modelo de regresión logística bivariado para la estimación de odds ratio (IC 95%) para HTA y multivariable ajustado por sexo, grupo etario, grupo étnico, estrato socioeconómico, hábito tabáquico y alcohólico, antecedente familiar de HTA, categorías de IMC, circunferencia abdominal alta, HDL-C baja, TAG alto, glicemia elevada, terciles del consumo diario de calorías y patrones de actividad física. Los datos obtenidos fueron analizados mediante el paquete informático SPSS versión 20, para Windows (SPSS Inc. Chicago, IL), se consideraron resultados significativos cuando el valor p fue menor de 0,05.

CONSIDERACIONES ÉTICAS

El protocolo del estudio fue evaluado y aprobado por el comité de ética del Centro de Investigaciones Endocrino-Metabólicas "Dr. Félix Gómez" de la Universidad del Zulia, como parte del desarrollo conjunto de una red de investigación multidisciplinaria para evaluar alteraciones endocrino-metabólicas en la ciudad de Cuenca, Ecuador. Los individuos que participaron en el estudio firmaron un consentimiento informado en el cual se expuso el respeto a la vida, la salud, la confidencialidad, la intimidad, la autonomía y la dignidad; asimismo, se les explicó todos los detalles concernientes al estudio y los procedimientos a los cuales iban a ser sometidos, antes de realizarles el examen clínico, físico y de laboratorio.

La muestra estuvo conformada por 318 individuos de los cuales el 57,2% (n=182) correspondió al sexo femenino. La edad media de la población general fue de 42,8 ± 15,5 años. Los grupos etarios más prevalentes fueron el de menos de 40 años con 44,7%, seguido del grupo de 40 a 59 años (39,0%) y 60 años o más con 16,4%. El grupo de individuos mestizos fue el grupo étnico más prevalente con un 96,2% (n=306). El resto de características generales se muestra en la Tabla 1.

La prevalencia total de HTA fue de 25,8% (n=82), el 14,8% (n=47) de la población presentó HTA conocida y un 11,0% (n=35) de la población fue diagnosticado como hipertenso durante el estudio. Al evaluar según sexo, se observó una prevalencia de HTA de 24,7% (n=45) en las mujeres y un 27,2% (n=37) en los hombres. La prevalencia de HTA según los grupos etarios, variables antropométricas y sociodemográficas se muestra en la Tabla 2, donde se muestra una asociación significativa entre el grupo etario y la HTA ( p<0,001), con un aumento en la prevalencia de HTA a medida que se incrementa la edad, desde un 12,0% en el grupo de menos de 40 años hasta un 53,8% en el grupo de 60 años y más. Por otra parte, se observó una asociación entre la HTA y el estatus socioeconómico ( p=0,001), con un aumento de la frecuencia de hipertensos a medida se incrementa el estrato (a partir del estrato II: 18,6%; estrato III: 19,8%; estrato IV: 27,5% y estrato V: 70,0%); no se evidenció una asociación significativa con el grupo étnico, condición laborar, patrones de actividad física o actividad física realizada en el tiempo de ocio por los sujetos ( Tabla 2).

Por otra parte, la presencia de antecedente familiar de HTA mostró una asociación significativa con la HTA, con un 30,9% de prevalencia de HTA aquellos sujetos con familiares de primer grado hipertensos ( p<0,05). La clasificación según IMC también mostró asociación con la presencia de HTA ( p<0,001) con una tendencia al aumento del porcentaje de HTA a medida que se incrementó de categoría de IMC, el grupo de menos de 25 kg/m ²: 16,4% (n=19); 25-29 kg/m ² (22,8%; n=29) y ≥30 kg/m ² (45,3%; n=75). Asimismo la HTA mostró una asociación con la presencia de obesidad abdominal ( p=0,010) ( Tabla 2).

En el modelo de regresión multivariable para la presencia de HTA, los factores asociados fueron el grupo de edad de 40-59 años (OR 2,66; IC 95%: 1,25-5,65; p=0,010) y ≥60 años (OR: 8,68; IC 95%: 1,25-21,14; p<0,001). Seguido de la presencia de obesidad por IMC (OR 2,36; IC 95%: 1,04-5,70; p=0,042). El resto de factores asociados fueron el alto consumo calórico y el antecedente familiar de HTA. Al analizar el consumo calórico como predictor de HTA, se observó que los sujetos con un consumo mayor o igual a 2471,94 kcal/24 h mostraron 2,06 veces mayor riesgo para HTA que los sujetos con un consumo menor a 1960,94 kcal/24 h (OR 2,06; IC 95%: 1,01-4,53; p=0,044) y los individuos con antecedente familiar de HTA presentaron 58% más riesgo para HTA que los sujetos sin antecedente de hipertensión (OR 1,58; IC 95%: 1,02-2,90; p=0,040) ( Tabla 2).

En el presente estudio se puede destacar que para la población de Cuenca los factores que ejercen mayor influencia para hipertensión arterial son la edad por encima de los 40 años, la presencia de obesidad de acuerdo al IMC, el antecedente familiar de HTA y la elevada ingesta calórica; por lo tanto, estos factores deben de ser abordados en la población para disminuir el riesgo a desarrollar HTA. Una limitante del presente estudio fue que no determinó la ingesta de sal como posible factor de riesgo para hipertensión arterial.

Los factores relacionados a la elevación de las cifras de PA varían entre las diferentes poblaciones y abarcan desde variables sociodemográficas hasta alteraciones específicas como trastornos endocrinos, renales e, incluso, consumo de ciertas sustancias o fármacos , la importancia en la identificación de estos factores radica en el potencial enfoque terapéutico cuando el trastorno o la sustancia es la causa desencadenante de la HTA, o cuando estas características acompañan a la elevación de las cifras de PA, interviniendo en su mecanismo fisiopatológico o incluso influyendo en la adherencia al tratamiento .

Es ampliamente conocido que el envejecimiento está acompañado de una serie de cambios metabólicos y degenerativos que afectan diversos órganos incluyendo la pared vascular , cuya rigidez y aumento progresivo de la resistencia a nivel periférico constituyen determinantes de suma importancia en el desarrollo o progresión de la HTA en los grupos etarios más longevos. Este comportamiento biológico hace necesario la exploración sistemática de este trastorno en la población adulta mayor, al observarse tendencias similares en diversas regiones del mundo 20. Pérez-Fernández R, Mariño AF, Cadarso-Suarez C, Botana MA, Tome MA, Solache I, et al. Prevalence, awareness, treatment and control of hypertension in Galicia (Spain) and association with related diseases. J Hum Hypertens. 2007;21(5):366-73. doi:10.1038/sj.jhh.1002158. ²⁰
https://doi.org/10.1038/sj.jhh.1002158...

21. Damasceno A, Azevedo A, Silva-Matos C, Prista A, Diogo D, Lunet N. Hypertension prevalence, awareness, treatment, and control in mozambique: urban/rural gap during epidemiological transition. Hypertension . 2009;54(1):77-83. doi: 10.1161/HYPERTENSIONAHA.109.132423.
https://doi.org/10.1161/HYPERTENSIONAHA....

22. Lee HS, Park YM, Kwon HS, Lee JH, Park YJ, Lim SY, et al. Prevalence, awareness, treatment, and control of hypertension among people over 40 years old in a rural area of South Korea: The Chungju Metabolic Disease Cohort (CMC) Study. Clin Exp Hypertens. 2010;32(3):166-78. doi: 10.3109/10641960903254497.
https://doi.org/10.3109/1064196090325449... ⁻.

Asimismo, estos hallazgos demuestran la presencia de factores intrínsecos y medioambientales asociados a un mayor riesgo de presentar HTA; previamente, se ha planteado que el antecedente familiar de esta alteración es un predictor importante en la aparición de cifras elevadas de PA , relacionado a diversos trastornos moleculares y fisiológicos que abarcan desde cambios en la elasticidad arterial hasta una activación simpática desde edades tempranas .

Entre los diversos factores ambientales evaluados, se observa que aquellos relacionados con el balance energético fueron los de mayor relevancia, siendo la obesidad determinada por IMC y el alto consumo calórico los más asociados a la presencia de HTA. En cuanto a la obesidad, nuestros resultados se asemejan a los obtenidos por Amira et al. , en sujetos de una comunidad urbana de Nigeria donde observaron que los pacientes obesos mostraban 2,6 veces más riesgo de ser hipertensos en comparación con los normopeso; sin embargo, a diferencia de nuestros hallazgos los individuos con sobrepeso también mostraron un mayor riesgo. Esto demuestra la importancia de intervenir de forma temprana en la población con sobrepeso de Cuenca, para evitar su progresión a obesidad, estado en el que podría iniciarse la agregación de factores de riesgo.

Por su parte, Raina et al. , también encontraron un alto grado de asociación entre ambas variables, a pesar de evidenciar una menor prevalencia de obesidad en más de 2000 sujetos adultos de una zona rural de la India. Los mecanismos involucrados en esta relación abarcan la activación del sistema nervioso simpático, del sistema renina-angiotensina-aldosterona, un aumento en la reabsorción de sodio, una progresiva disfunción endotelial e insulinorresistencia; los cuales representan blancos terapéuticos a considerar en la instauración de la terapia farmacológica .

Sin embargo, más allá del uso de fármacos antihipertensivos, es importante destacar el papel de los cambios en el estilo de vida no solo como factor involucrado en el control de las cifras de PA sino también en su aparición. Específicamente, los hábitos nutricionales, los cuales en nuestra población parecen relacionarse con HTA de forma independiente al desarrollo de obesidad, lo cual confirma la importancia de los hábitos psicobiológicos en la prevalencia y prevención de esta enfermedad evidenciada en reportes previos ,.

Al igual de lo planteado por Mathew et al. , en una población hindú, el consumo calórico excesivo constituye en la ciudad de Cuenca, un factor íntimamente relacionado al desarrollo o precipitación de la HTA, por lo cual resulta necesario establecer políticas en salud orientadas a informar a los profesionales de la salud y población general que un consumo calórico diario superior a las 2500 calorías se relaciona a un mayor riesgo de presentar cifras elevadas de PA.

Entre las limitaciones respectivas al tipo de estudio realizado, el diseño transversal imposibilita establecer relaciones de causalidad, para lo cual se necesitan futuros análisis prospectivos que realicen seguimiento de estos sujetos y de los factores de riesgo cardiovascular potenciales que pueden agregarse en caso de no seguir las medidas terapéuticas adecuadas, así como de los potenciales factores que influyen en el adherencia al tratamiento.

En conclusión, los principales factores asociados a la presencia de HTA en la población adulta de la ciudad de Cuenca, Ecuador, fueron la edad, la presencia del antecedente familiar, obesidad y un alto consumo calórico, los cuales deben considerarse y evaluarse de forma sistémica en los pacientes adultos que consulten en nuestra localidad, con el fin de brindar un diagnóstico temprano y un tratamiento integral desde etapas tempranas

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Factores de riesgo para hipertensión arterial en población adulta de una región urbana de Ecuador

# data[].attributes.attachment_link.description
Entre los diversos factores de riesgo para las enfermedades cardiovasculares (ECV), la hipertensión arterial (HTA) es considerada uno de los más importantes a nivel mundial, asociándose a eventos coronarios y cerebrovasculares en aproximadamente 60 y 77% de los casos, respectivamente .

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TITULO: Caracterización clínica- epidemiológica de la hipertensión arterial

TIPO DE ESTUDIO: Estudio descriptivo

AÑO: 2019

RESULTADO: Del total de pacientes, 48,7 % pertenecía al grupo de edad 40 y 59 años. Predominaron las féminas (112/58,03 %) y los pacientes de piel negra (36,8 %). El factor de riesgo modificable que predominó fue el tabaquismo, presente en 62,7 %; 55,4 % presentó cifras de tensión arterial controladas. La mayoría usaba 2 fármacos antihipertensivos (44,6 %).

CONCLUSIONES: La hipertensión arterial en el adulto es mejor controlada a menor edad y cuando se utilizan dos fármacos. El principal factor de riesgo de los hipertensos fue el tabaquismo.
La presión sistólica se incrementa con la edad, principalmente por pérdida de la elasticidad de las grandes arterias; además, existe un incremento de estímulos vasoconstrictores potenciados por el incremento del grosor de la capa media y la masa ventricular.

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tipo : metaanálisis
año: 2015
título: Estado socioeconómico e hipertensión
Resultados: Se encontró aumento general del riesgo de hipertensión según los niveles socioeconómicos: indicadores ingresos, ocupación y educación. Las asociaciones fueron significativas en los países de altos ingresos, y el mayor riesgo de hipertensión para las categorías más bajas de todos los indicadores SES fue más evidente para las mujeres, mientras que los hombres revelaron asociaciones menos consistentes.

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national center for biotechnology information

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PubMed® comprises more than 36 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full text content from PubMed Central and publisher web sites.

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https://scielo.isciii.es/scielo.php?script=sci_arttext&pid=S1695-61412012000200022

Hipertensión arterial: principales factores de riesgo
Este artículo tiene como objetivo el estudio de los principales factores de riesgo de la hipertensión arterial. Se observó la necesidad de valoración de nuevos conceptos de salud-enfermedad y participación del usuario de salud en la elaboración de un plan de intervención, con estímulo al abandono del consumo de tabaco y del uso abusivo de alcohol, reducción de peso entre aquellos con sobrepeso, implementación de actividades físicas, reducción del consumo de sal, aumento del consumo de hortalizas y frutas, además de la disminución en el consumo de alimentos grasos, entre otros, para estimular el auto-cuidado promoviendo una mejora en la calidad de vida de la población.

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En este estudio se realizó un diseño descriptivo de corte transversal para analizar cómo influyen los factores de riesgo predictivos de la enfermedad cardiovascular en la población pediátrica.  En las edades analizadas, predominó el color de la piel no blanca, se determinó que el peso, la talla y el índice de masa corporal, de forma aislada, no son buenos predictores para la tensión arterial.  algunos presentaron síntomas muy sutiles que incluso pueden ser atribuidos a otras enfermedades, y la circunferencia de la cintura fue el marcador antropométrico de más relevancia asociado a los niños hipertensos.

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1. Según los criterios del JNC.

El Comité Nacional Conjunto Americano en Detección, Evaluación y Tratamiento de la HTA (JNC) agrupó en 1993 la HTA en 4 niveles o categorías, tomando en igual consideración tanto la PAD como la PAS. (Valero R, García S,. 2009)

LINK DEL ARTICULO: https://revistas.um.es/eglobal/article/view/50131/48911

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La hipertensión arterial (HTA) se mantiene como un importante problema de salud pública a nivel mundial. En este estudio se menciona que constituye la primera causa de morbimortalidad y el factor de riesgo con mayor carga de riesgo atribuible para cardiopatía isquémica y accidente cerebrovascular.

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RESUMEN

La Hipertensión Arterial (HTA) continúa siendo un problema de Salud Pública relevante a nivel mundial. En Chile es la principal causa de morbimortalidad y el factor de riesgo de mayor carga atribuible para la patología cardiovascular isquèc)mica y el accidente cerebrovascular. En este artículo se revisa su prevalencia, el grado de conocimiento, el logro de su control y tratamiento, así como su riesgo atribuible analizando la carga de enfermedad y la pèc)rdida de años por discapacidad. Se presentan estudios del impacto de su inclusión en el AUGE, resultados de la intervención multidisciplinaria, su interacción con otros factores de riesgo cardiovascular y se comentan algunos aspectos de las actualizaciones de las guías internacionales para su manejo.

SUMMARY

Hypertension (HT) remains as an important public health problem worldwide. In Chile constitutes the leading cause of morbidity and mortality and the risk factor with the highest attributable risk burden for ischemic heart disease and stroke. This article reviews HT́s prevalence, degree of knowledge, achievement of its control and treatment. Also the risk burden of disease and disability loss years due to this pathology is analyzed. The results of studies after the inclusion of HT as explicit guaranteed health problem, multidisciplinary approach and its interaction with other cardiovascular risk factors is presented. Finally, some aspects of international updates guidelines for its management are discussed.

Keywords

guidelines.

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IMPACTO DE LA HIPERTENSIÓN ARTERIAL COMO FACTOR DE RIESGO CARDIOVASCULAR

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La Hipertensión Arterial (HTA) continúa siendo un problema de Salud Pública relevante a nivel mundial. En Chile es la principal causa de morbimortalidad y el factor de riesgo de mayor carga atribuible para la patología cardiovascular isquèc)mica y el accidente cerebrovascular.

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Con base en un análisis de datos de 135 estudios basados ​​en la población que incluyeron a 968 419 adultos de 90 países, estimamos que en 2010 la prevalencia global de hipertensión estandarizada por edad (definida como PA sistólica ≥140 mm Hg, PA diastólica ≥90 mm Hg, y/o uso actual de medicación antihipertensiva) fue del 31,1 % (IC del 95 %: 30,0–32,2 %).

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En este articulo menciona que   la   población   afroamericana,   factores

como la alta sensibilidad a la sal, bajos

niveles  de  renina  y    la  sobreexpresión

de la Endotelina 1 inciden directamente

en  la  alta  prevalencia  de  hipertensión

arterial   (HTA)   y   de   daño   a   órgano

blanco

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Vista de Hipertension arterial en personas de raza negra | Revista Medica Sinergia

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https://pubmed.ncbi.nlm.nih.gov/31859886/#:~:text=The%20standardized%20prevalence%20of%20HBP,(24.2%20vs%2012.9%20respectively)

Cambios en la prevalencia de hipertensión arterial en el Perú según la nueva guía del Colegio Americano de Cardiología.

Métodos: Estudio transversal de la Encuesta Demográfica y de Salud Familiar realizada en Perú en 2017. Se estimaron prevalencias de hipertensión ponderadas estandarizadas para la población de la OMS según ambas guías, y diferencias absolutas con IC 95%.

Resultados: Se incluyeron 30.682 personas de 18 años y más, con una edad media de 42,3 años, 51,1% mujeres. La prevalencia estandarizada de HTA para el año 2017 según JNC 7 fue de 14,4% (IC 95%: 13,8-15,1) y según ACC/AHA 2017 fue de 32,9% (IC 95%: 32,0-33,7), por lo que el aumento de prevalencia es de 18,5 puntos porcentuales, siendo mayor en hombres que en mujeres (24,2 vs 12,9 respectivamente). En las personas con obesidad y/o que consumen tabaco, los incrementos fueron mayores (24,3 y 24,1 puntos porcentuales respectivamente). En las regiones de Tacna, Ica y Lima Metropolitana, el incremento, en comparación con los lineamientos de la JNC 7, superó el promedio nacional (22,4, 20,7 y 20,4 puntos porcentuales, respectivamente).

Conclusiones: Considerando el contexto de un país latinoamericano y conociendo la epidemiología de la hipertensión arterial en Perú, la potencial adopción de las guías ACC/AHA 2017 para la prevención, detección, evaluación y manejo de la hipertensión arterial debe ir acompañada de una evaluación del impacto a nivel individual, sistémico y social.

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[Changes in the prevalence of hypertension in Peru using the new guideline of the American College of Cardiology] - PubMed

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Considering the context of a Latin American country and knowing the epidemiology of hypertension in Peru, the potential adoption of the ACC/AHA 2017 guidelines for the prevention, detection, evaluation, and management of hypertension should be accompanied by an evaluation of the impact at the indivi…

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Etiología
- Mala calidad de sueño.
- Apnea del sueño.
- Estrés mental elevado.
- Ingesta insuficiente de potasio.
- Inactividad
- Entorno intrauterino adverso.

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Nat Rev Dis Primers. Author manuscript; available in PMC 2019 Apr 23.

Published in final edited form as:

Suzanne Oparil, ¹ Maria Czarina Acelajado, ² George L. Bakris, ³ Dan R. Berlowitz, 4, ⁵ Renata Cífková, ⁶ Anna F. Dominiczak, ⁷ Guido Grassi, 8, ⁹ Jens Jordan, ¹⁰ Neil R. Poulter, ¹¹ Anthony Rodgers, ¹² and Paul K. Whelton ¹³

Abstract

Systemic arterial hypertension is the most important modifiable risk factor for all-cause morbidity and mortality worldwide and is associated with increased risk of cardiovascular disease (CVD). Fewer than half of those with hypertension are aware of their condition, and many others are aware but not treated or inadequately treated, although successful treatment of hypertension reduces the global burden of disease and mortality. The aetiology of hypertension involves the complex interplay of environmental and pathophysiological factors that affect multiple systems, as well as genetic predisposition. Evaluation of patients with hypertension includes accurate standardized blood pressure (BP) measurement, assessing patients' predicted risk of atherosclerotic CVD, evidence of target organ damage, detection of secondary causes of hypertension and presence of comorbidities, including CVD and kidney disease. Lifestyle changes, including dietary modifications and increased physical activity, are effective in lowering BP and preventing hypertension and its CVD sequelae. Pharmacological therapy is very effective in lowering BP and preventing CVD outcomes in most patients; first line antihypertensive medications include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, dihydropyridine calcium channel blockers and thiazide diuretics.

INTRODUCTION

Systemic arterial hypertension (hereafter referred to as hypertension) is characterized by persistently high blood pressure (BP) in the systemic arteries. BP is commonly expressed as the ratio of the systolic BP (that is, the pressure that the blood exerts on the arterial walls when the heart contracts) and the diastolic BP (the pressure when the heart relaxes). The BP thresholds that define hypertension depend on the measurement method ( Table 1 ). Several aetiologies can underlie hypertension. The majority (90-95%) of patients have a highly heterogeneous 'essential' or primary hypertension with a multifactorial gene-environment aetiology. A positive family history is a frequent occurrence in patients with hypertension, with the heritability (a measure of how much of the variation in a trait is due to variation in genetic factors) estimated between 35% and 50% in the majority of studies1,2. Genome-wide association studies (GWAS) have identified ~120 loci that are associated with BP regulation and together explain 3.5% of the trait variance3,4,5. These findings are becoming increasingly important as we search for new pathways and new biomarkers to develop more-modern 'omics'-driven diagnostic and therapeutic modalities for hypertension in the era of precision medicine6.

Table 1 -

Category

Subtype

Systolic BP (mmHg)

Diastolic BP (mmHg)

Office BP

NA

≥ 140

≥ 90

Ambulatory BP

Daytime (awake)

≥ 135

≥ 85

Night time (asleep)

≥ 120

≥ 70

24hr

≥ 130

≥ 80

Home BP

NA

≥ 135

≥ 85

Several rare, monogenic forms of hypertension have been described (for example, the Liddle syndrome, glucocorticoid-remediable aldosteronism (a mineralocorticoid excess state) and mutations in PDE3A (which encodes cGMP-inhibited 3',5'-cyclic phosphodiesterase A)), in which a single gene mutation fully explains the pathogenesis of hypertension and indicates the best treatment modality7,8,9. If hypertension is caused by another condition (for example, primary aldosteronism, pheochromocytoma (a neuroendocrine tumour of the adrenal glands or other neuroendocrine tissues) or renal artery stenosis), it is referred to as secondary hypertension.

Hypertension is the most common preventable risk factor for cardiovascular disease (CVD; including coronary heart disease, heart failure, stroke, myocardial infarction, atrial fibrillation and peripheral artery disease), chronic kidney disease (CKD) and cognitive impairment, and is the leading single contributor to all-cause death and disability worldwide10. The relationship between BP and the increased risk of CVD is graded and continuous, starting as low as 115/75 mmHg, well within what is considered to be the normotensive range. Successful prevention and treatment of hypertension are key in reducing disease burden and promoting longevity in the world's population. In treating hyperteinsion, it is important to consider a person's predicted atherosclerotic CVD (ASCVD) risk more than the level of BP alone, as persons with high CVD risk derive the greatest benefit from BP lowering treatment11.

This Primer will discuss the epidemiology and pathophysiology of primary hypertension, prevention strategies for slowing the progression of BP elevation, management strategies (including optimal BP targets) for lowering BP and preventing CVD outcomes in patients with established hypertension and the effects of antihypertensive treatment on quality of life; finally, we will explore knowledge gaps, future trends and the outlook for hypertension research and treatment over the next decade.

EPIDEMIOLOGY

As economic development progresses, hypertension initially affects those with a high socioeconomic status, but at later stages of economic development, the prevalence of hypertension and its consequences are greatest in those with lower socioeconomic status; this phenomenon is seen both within and between countries. Further, the speed of change prevalence of hypertension since 2000 to 2010 has been much more rapid than in previous epidemiological transitions15.

Disease burden

Globally, 3.5 billion adults now have non-optimal systolic BP levels (that is, >110-115 mmHg) and 874 million adults have systolic BP ≥140 mmHg. Thus, approximately one in four adults has hypertension16. Between 1990 and 2015 there was a 43% increase in the total global number of healthy life years lost to non-optimal BP, driven by population increase, population aging and a 10% increase in the age-standardized prevalence of hypertension16. The Global Burden of Disease study has shown that non-optimal BP continues to be the biggest single risk factor contributing to the global burden of disease and to global all-cause mortality, leading to 9.4 million deaths and 212 million lost healthy life years (8.5% of the global total) each year10.

CVD risk

Prospective observational studies have repeatedly demonstrated a strong, continuous positive relationship between BP and CVD, with no evidence of a threshold for risk throughout the usual range of BP observed in clinical practice. The relationship between BP and CVD applies to both systolic BP and diastolic BP, but is somewhat more robust for systolic BP in adults19. It is noted in both sexes, at all ages throughout adulthood and for all major manifestations of CVD, including stroke (ischaemic and haemorroagic), coronary artery disease, heart failure, peripheral vascular disease and end stage renal disease (although there are variations in the strength of the associations and the slopes of the curves)17,18,19,20 ( Figure 1 ). The relationship is independent of other CVD risk factors, and level of BP has proven to be a major component of CVD risk in all prediction models21. Approximately two-thirds of all adults who have hypertension or receive treatment with BP lowering medication at 30 years of age have a ~40 % higher risk of experiencing a CVD event than their age-matched and sex-matched counterparts with a lower level of BP18. In addition, CVD events in individuals with hypertension tend to manifest about five years earlier than in individuals with a lower level of BP18.

In individuals of 40-69 years of age, a 20 mmHg rise of systolic BP or a 10 mmHg rise of diastolic BP regardless of baseline values is associated with more than a doubling of the risk for stroke or ischaemic heart disease mortality17, whereas a systolic BP reduction of 5 mmHg can decrease stroke mortality by 14% and CVD mortality by 9%. At older ages (≥80 years), the corresponding relative risk is slightly lower, but the absolute risk is far greater than earlier in life17. For example, a 20 mm Hg difference in systolic BP between 120 and 140 mmHg is associated with an annual difference in absolute risk that is nearly ten times larger at ages 80-89 years than that at ages 50-59 years17.

MECHANISMS/PATHOPHYSIOLOGY

BP regulation

BP is determined by several parameters of the cardiovascular system, including blood volume and cardiac output (the amount of blood pumped by the heart per minute) as well as the balance of arterial tone that is affected by both intravascular volume and neurohumoral systems (discussed in the following sections). The maintenance of physiological BP levels involves a complex interplay of various elements of an integrated neurohumoral system that includes the renin-angiotensin-aldosterone system (RAAS), the role of natriuretic peptides and the endothelium, the sympathetic nervous system (SNS) and the immune system ( Figure 2 ). Malfunction or disruption of factors involved in BP control in any of these systems can directly or indirectly lead to increases in mean BP, BP variability or both, over time resulting in target organ damage (for example, left ventricular hypertrophy and CKD) and CVD outcomes22.

The pathophysiological mechanisms responsible for hypertension are complex and act on a genetic background. Primary hypertension involves multiple types of genes; some allelic variants of several genes are associated with an increased risk of developing primary hypertension and are linked in almost all cases to a positive family history ( Box 1) This genetic predisposition, along with a host of environmental factors, such as high Na⁺ intake, poor sleep quality or sleep apnoea, excess alcohol intake and high mental stress, contribute to the development of hypertension. Finally, the probability of developing hypertension increases with aging, owing to progressive stiffening of the arterial vasculature caused by, among other factors, slowly developing changes in vascular collagen and increases in atherosclerosis. Immunological factors can also play a major part, especially on the background of infectious or rheumatological diseases such as rheumatoid arthritis. The mosaic theory of hypertension describes its multifaceted pathophysiology28,29.

Box 1.

A large GWAS of 2.5 million genotyped single nucleotide polymorphisms (SNPs) in >69,000 individuals of European ancestry from 29 studies demonstrated that most SNPs related to BP regulation and CVD risk involved natriuretic peptides198. SNPs in genes that encode precursors for ANP and BNP had been previously identified199, and two other loci were identified in this study, containing genes involved in natriuretic peptide and NO signalling pathways; both these pathways regulate cyclic guanosine monophosphate, which promotes vasodilation. A 2016 study identified 66 BP-associated loci, which were enriched for cis-regulatory elements in vascular endothelial cells, consistent with a role in BP control through modulation of vascular tone. This information prompted development of a genetic risk score to predict target organ damage4.

Gene deletion studies in rodent models have evaluated cardiac ANP and BNP as paracrine regulators of vascular regeneration. Deletion of the genes encoding ANP and BNP exaggerates cardiac fibrosis and increase adverse left ventricular (LV) remodelling38, and natriuretic peptide receptor A (NPRA) deficiency leads to increased BP, severe fibrosis and LV dysfunction. Further, deletion of the gene encoding the endothelial guanylyl cyclase-A (GC-A) receptor, a cell surface receptor for natriuretic peptides, leads to diminished vascular regeneration and angiogenesis in response to critical hind limb ischemia, as well as cardiac fibrosis and diastolic dysfunction.

Further, clinical studies have observed an association between certain corin gene polymorphisms and risk of pre-eclampsia and hypertension, particularly among African-American but not Chinese populations200.

Sodium homeostasis regulation

Sodium (Na⁺) is a crucial regulator of blood volume: high serum Na⁺ concentration promotes fluid (water) retention, thereby increasing blood volume and BP. When dietary Na⁺ increases in normotensive individuals, compensatory haemodynamic changes occur to maintain constant BP. These changes include reduction in renal and peripheral vascular resistance and increased production of nitric oxide (a vasodilator) from the endothelium. However, if the effect of nitric oxide is impaired or absent, an increase in BP occurs. Endothelial dysfunction is a risk factor for the development of salt sensitivity and subsequent hypertension. Salt sensitivity is defined as a marked elevation in BP following a Na⁺ load of ≥5 g and is characterized by an elevation of systolic BP of at least 10 mmHg within a few hours of ingestion. Salt sensitive individuals have underlying endothelial dysfunction due to genetic or environmental influences. In response to a high salt load these individuals generally manifest overproduction of transforming growth factor β (TGF-β), which increases the risk of fibrosis, and oxidative stress, and have limited bioavailable nitric oxide. Chronic high salt ingestion can result in endothelial dysfunction, even in salt-resistant individuals30, and also affects the gut microbiota, with resultant changes that contribute to increased salt sensitivity and the development of hypertension31. High salt intake also appears to drive autoimmunity by inducing T helper 17 (T H17) cells31. High salt intake in mice has been shown to deplete Lactobacillus murinus in the gut microbiota. Treatment of mice with L. murinus prevented salt-induced exacerbation of salt-sensitive hypertension by modulating T H17 cells31. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased the activity of T H17 cells and increased BP31. Thus, the gut microbiota appears to contribute to salt sensitivity of BP and the pathogenesis of hypertension.

Renin-Angiotensin-Aldosterone System

The RAAS has wide-ranging effects on BP regulation, mediating Na⁺ retention, pressure natriuresis (that is, the mechanism whereby increases in renal perfusion pressure (the gradient between renal arterial and venous blood pressure) lead to decreased Na⁺ reabsorption and increased Na⁺ excretion), salt sensitivity, vasoconstriction, endothelial dysfunction and vascular injury, and plays an important part in the pathogenesis of hypertension22. The RAAS is present at the cellular level in many organs, but its most crucial role is to help regulate pressure-volume homeostasis in the kidney, where it maintains perfusion in volume depleted states (that is, when there is a reduction in extracellular fluid volume as a result of sodium and fluid loss) and is suppressed in volume expanded (fluid overload) conditions. Renin and its precursor pro-renin are synthesized and stored in the juxtaglomerular cells of the kidney and are released in response to various stimuli ( Figure 3 ). The main function of renin is to cleave angiotensinogen to form angiotensin I. Angiotensin-converting enzyme (ACE) cleaves angiotensin I to form angiotensin II, which is at the center of the pathogenetic role of the RAAS in hypertension ( Figure 3 )32..

Angiotensin II enhances Na⁺ reabsorption in the proximal tubule by increasing the activity of the sodium-hydrogen exchanger (NHE3), sodium-bicarbonate exchanger and sodium-potassium ATPase, and by inducing aldosterone synthesis and release from the adrenal glomerulosa22. Angiotensin II is also associated with endothelial dysfunction and has pro-fibrotic and pro-inflammatory effects, mediated in large part by increased oxidative stress, resulting in renal, cardiac and vascular injury. Angiotensin II is tightly linked to target organ damage in hypertension via these mechanisms22..

Angiotensin-converting enzyme 2 (ACE2) has emerged as an important modulator in the pathophysiology of hypertension, CVD and renal disease, owing to its role in metabolizing angiotensin II into angiotensin-(1-7)33. Ang-(1-7) induces systemic and regional vasodilation, diuresis and natriuresis, and exerts antiproliferative and antigrowth effects on vascular smooth muscle cells, cardiac myocytes and fibroblasts as well as glomerular and proximal tubular cells33. Ang-(1-7) also has cardiorenal protective effects that are mediated by the proto-oncogene Mas receptor through signalling pathways that include mitogen-activated protein kinases (MAPK), PI3K-AKT, NADPH oxidase, TGF-β1, the EGF receptor, and NF-κB activity.

Aldosterone plays a crucial part in hypertension: by binding to the mineralocorticoid receptor, it induces non-genomic effects (that is, without directly modifying gene expression) that include activation of the amiloride-sensitive sodium channel, commonly known as the epithelial sodium channel (ENaC) and result in the stimulation of renal Na⁺ reabsorption in the cortical collecting duct36. Aldosterone also has many non-epithelial effects that contribute to endothelial dysfunction, vasoconstriction and hypertension36,37. These include vascular smooth muscle cell proliferation, vascular extracellular matrix deposition, vascular remodeling, fibrosis, and increased oxidative stress36,37.

Natriuretic Peptides

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) play an important part in salt sensitivity and hypertension. They have important natriuretic and vasodilator properties that allow maintenance of Na⁺ balance and BP during Na⁺ loading38,39. Upon administration of a Na⁺ load, atrial and ventricular stretch leads to release of ANP and BNP, respectively, which leads to systemic vasodilation and decreased plasma volume (owing to fluid shifts from the intravascular to the interstitial compartment) and results in BP lowering40. Natriuretic peptides increase glomerular filtration rate via an increase in efferent arteriolar tone in volume-expanded states and inhibit renal Na⁺ reabsorption through both direct and indirect effects. Direct effects include decreased activity of Na⁺-K⁺-ATPase and the sodium-glucose co-transporter in the proximal tubule and inhibition of the epithelial sodium channel in the distal nephron. Indirect effects include inhibition of renin and aldosterone release39.

Natriuretic peptide deficiency promotes hypertension. Corin is a serine protease that is largely expressed in the heart and converts the ANP and BNP precursors pro-ANP and pro-BNP to their active forms. Corin deficiency has been associated with volume overload, heart failure and salt-sensitive hypertension41. Natriuretic peptide deficiency also predisposes to insulin resistance and type 2 diabetes mellitus. Obesity is associated with natriuretic peptide deficiency, probably through upregulation of the natriuretic peptide scavenger receptor NPR-C in adipose tissue42. Natriuretic peptides have therapeutic potential for the metabolic syndrome; the metabolic syndrome is a cluster of conditions (including high BP, high fasting glucose levels, abdominal obesity, high triglycerides and microalbuminuria) that occur together, increasing the risk of CVD and diabetes mellitus42.

The Endothelium

The endothelium is a major regulator of vascular tone and major contributor to salt sensitivity through NO. Endothelial cells produce a host of vasoactive substances, of which NO is the most important in BP regulation43,44. NO is continuously released by endothelial cells in response to flow-induced shear stress, leading to vascular smooth muscle relaxation through activation of guanylate cyclase and generation of intracellular cyclic guanosine monophosphate45. Interruption of NO production via inhibition of constitutively expressed endothelial NO synthase (eNOS) causes BP elevation and development of hypertension in animals and humans46. Studies to evaluate NO activity in humans have demonstrated decreased whole-body production of NO in patients with hypertension compared with normotensive controls46,47.

Endothelial cells also secrete a variety of other vasoregulatory substances, including vasodilators such as prostacyclin and endothelium-derived hyperpolarizing factors, and vasoconstrictors such as endothelin 1 (ET-1), locally generated angiotensin II and the prostanoids thromboxane A2 and prostaglandin A2. ET-1 is a potent vasoconstrictor that activates ET-A receptors in vascular smooth muscle48. Other vasodilating substances, secreted by a variety of cells types, such as calcitonin gene related peptide, adrenomedullin and substance P act primarily through increases in NO release from endothelial cells49,50. The glucose-regulating gut hormone glucagon-like peptide-1 (GLP-1) also has vasodilating properties51. The balance between these factors, along with NO and ET-1, determines the final effect of the endothelium on vascular tone52,48,53,51. Circulating ET-1 levels are not consistently increased in hypertension, but there is a trend toward increased sensitivity to the vasoconstrictor and hypertensive effects of ET-1 in individuals with hypertension53. ET-A receptor antagonists attenuate or abolish hypertension in a variety of experimental models and are effective in lowering BP in humans48,53.

Endothelial dysfunction plays a seminal part in the pathogenesis of hypertension. Normotensive offspring of parents with hypertension often have impaired endothelium-dependent vasodilation, which implies a genetic component in the development of endothelial dysfunction47. Endothelial dysfunction in the setting of chronic hypertension is related to a combination of direct pressure-induced injury and increased oxidative stress. Several enzyme systems, including NADPH oxidase, xanthine oxidase and cyclooxygenase, as well as decreased activity of superoxide dismutase generate reactive oxygen species47,54. Excess superoxide anions bind to NO, decreasing NO bioavailability and generating the pro-inflammatory oxidant, peroxynitrite. Decreased NO bioavailability is the central factor that links oxidative stress to endothelial dysfunction and hypertension47. Salt-sensitive individuals may be very sensitive to the hemodynamic stress of increased blood volume, leading to overproduction of TGF-beta, oxidative stress, and limiting bioavailable NO30. Angiotensin II, along with other factors, including cyclic vascular stretch as a result of BP changes, endothelin-1 (ET-1), uric acid, systemic inflammation, norepinephrine, free fatty acids, and tobacco smoking, enhances NADPH oxidase activity and plays a central part in the generation of oxidative stress in hypertension52.

Sympathetic Nervous System

Baroreceptors, mechanoreceptors that sense pressure changes of the circulatory system, are housed in various locations in the arterial tree, a key place being the carotid sinus, a dilated area at the base of the internal carotid artery just superior to bifurcation of the common carotid artery. When this artery is stretched by elevated BP, nerve bundles projecting from the baroreceptors in the carotid sinus send messages to the brain to reduce sympathetic outflow of nerve impulses or nerve traffic and, thereby, BP. The SNS is generally more activated in persons with hypertension than in normotensive individuals.58,59 SNS activity is also greater in individual with obesity, in men than in women, in younger than in older persons, and in those with advanced kidney disease.60,61 Many patients with hypertension are in a state of autonomic imbalance with increased sympathetic and decreased parasympathetic activity59,62. SNS hyperactivity is relevant to both the generation and maintenance of hypertension. Studies in humans have also identified markers (such as increased catecholamine spillover and sural nerve activity assessed by microneurography) of sympathetic overactivity in normotensive individuals with a family history of hypertension63. Among patients with hypertension, increasing severity of hypertension is associated with increasing levels of sympathetic activity measured by microneurography64,65. Plasma catecholamine levels, microneurographic recordings and systemic catecholamine spillover (the amount of catecholamines released from sympathetic nerves innervating blood vessels that enter the bloodstream) studies have given evidence of increased sympathetic activity in patients with hypertension who are obese, in those with the metabolic syndrome, and in those whose hypertension is complicated by heart failure or kidney disease65.

The importance of the SNS in the pathogenesis of hypertension has been defined in a variety of experimental models. Models of obesity-related hypertension demonstrate that increased renal sympathetic nerve activity and its attendant increase in renal sodium reabsorption are key factors in the maintenance of sustained hypertension62. In another animal model, rats that received daily infusions of phenylephrine for 8 weeks developed hypertension during the infusions; their BP normalized under a low salt diet after discontinuation of phenylephrine, but once re-challenged with a high salt diet, the animals became hypertensive again30. The degree of BP elevation on the high salt diet was directly related to the degree of renal tubulo-interstitial fibrosis and decrease in glomerular filtration rate, suggesting that catecholamine-induced hypertension causes renal interstitial injury and a salt-sensitive phenotype that persists even after sympathetic overactivity is no longer present. In addition, enhanced SNS activity results in alpha-1 adrenergic receptor mediated endothelial dysfunction, vasoconstriction, vascular smooth muscle proliferation and increased arterial stiffness, which contribute to the development and maintenance of hypertension66. Finally, there is evidence that sympathetic overactivity enhances salt-sensitivity owing to a reduction in activity of the WNK lysine deficient protein kinase 4 ( WNK4) gene, which encodes a serine/threonine kinase that inhibits the thiazide-sensitive-Na-Cl co-transporter, resulting in increased distal tubular Na⁺ retention67. These mechanisms have been reviewed recently66.

Inflammation and the immune system

Inflammation makes an important contribution to the genesis of hypertension and related target organ damage. Inflammation is associated with increased vascular permeability and release of potent mediators, such as reactive oxygen species, NO, cytokines and metalloproteinases. Cytokines mediate the formation of neo-intima (a new or thickened layer of arterial intima), thereby decreasing the lumen diameter of resistance vessels (small arteries and arterioles highly innervated by autonomic nerves and the primary vessels involved in the regulation of BP), and promoting vascular fibrosis, leading to increased vascular resistance and stiffness. Cytokines also affect renal tubular function by increasing local synthesis of angiotensinogen and angiotensin II, as well as promoting sodium and volume retention in hypertension68. Matrix metalloproteinases stimulate the degradation of the extracellular matrix, allowing infiltration of immune cells through the vessel wall into the interstitium of the affected organs, promoting apoptosis and enhancing collagen synthesis and matrix deposition, leading to target organ damage68.

While animal data are clear about the relationship between inflammation and hypertension, the data in humans are limited. There are associations between C-reactive protein, TNF-alpha and various interleukins and hypertension, but no direct link68. GWASs have identified a single nucleotide polymorphism of SH2B3 (SNP rs3184504), which results in an amino acid substitution in SH2B adapter protein 3 (a protein involved in T cell receptor activation and signalling), that is associated with many autoimmune and cardiovascular disorders, including hypertension69. Further, drugs that are used to treat inflammation, such as non-steroidal anti-inflammatory drugs and cyclosporine, raise rather than lower BP in hypertensive individuals, highlighting the complex nature of the relationship between inflammation and hypertension69.

Both innate and adaptive immune responses participate in the generation of reactive oxygen species and inflammatory changes in the kidneys, blood vessels and brain in hypertension68,70. Innate immune responses, especially those mediated by macrophages, have been linked to hypertension induced by angiotensin II, aldosterone and NO antagonism68,70. Reductions in macrophage infiltration of the kidney or the peri-adventitial space of the aorta and medium sized arteries lead to reductions in BP and salt-sensitivity68. Adaptive immune responses via T cells have also been linked to the genesis of hypertension and its target organ damage. T cells express AT1 receptors and mediate angiotensin II-dependent hypertension,70 and it has been shown that depletion of mature lymphocytes ameliorated hypertension and kidney injury resulting from a high-salt diet in the Dahl SS rat71. Thus, a balance between proinflammatory T cell reactivity and inflammatory suppression induced by T regulatory cells determines the development of hypertension, as demonstrated by the amelioration of hypertension with the adoptive transfer of T regulatory cells in several animal models of hypertension68-70. Abnormalities in both pro-inflammatory T cells and regulatory T cells are implicated in hypertension-induced target organ damage, as they regulate the inflammatory processes in the kidney and vasculature that underlie hypertension-induced kidney disease

DIAGNOSIS, SCREENING AND PREVENTION

Diagnosis and screening

Essential or primary hypertension is usually asymptomatic; thus, in clinical practice all adults should have their BP measured at regular office visits. Hypertension is most commonly diagnosed based on repeated BP measurements in a clinical office setting. Accurate measurement and recording of BP is essential to categorize the level of BP, ascertain BP-related CVD risk and guide management. Since 2010, methods to measure out-of-office BP have been increasingly introduced to guide diagnosis and treatment of hypertension72,73. Table 1 These include home BP monitoring (HBPM) and ambulatory BP monitoring (ABPM). HBPM refers to the measurement of BP at regular intervals by an individual at their home or elsewhere outside the clinic setting. ABPM consists of measuring and recording the BP at regular intervals (usually every 20-30 minutes), typically for the 24-hour period and while individuals go about their daily activities. The ability to measure out-of-office BP has enabled the identification of distinct BP phenotypes, including white coat or isolated clinic hypertension and masked or isolated ambulatory hypertension74,75. White coat hypertension is characterised by elevated office BP but normal ABPM or HBPM readings. By contrast, masked hypertension is characterised by normal office readings but elevated out -of-office readings ( ABPM and HBPM )74,75.

Diagnosis

The evaluation of a patient with hypertension requires more than the diagnosis of elevated BP. It should also include assessment of the CVD risk, target organ damage, and concomitant clinical conditions that may affect the BP or related target organ damage as well as recognition of features suggestive of secondary hypertension. Some of these investigations are routine tests necessary in all patients, but others only in specific patient groups identified by history, clinical examination, and routine tests. In rare inherited forms of hypertension, a single gene mutation explains the pathogenesis of hypertension7,8,9. ( Figure 4 ) A small proportion of patients have a potentially reversible cause of hypertension, and a correct diagnosis might lead to a cure or a substantial improvement in BP control with a reduction of CVD risk. It is therefore appropriate to implement a simple screening for secondary hypertension in all patients. The screening is based on clinical history, physical examination and routine laboratory investigations ( Box 2 and 3). Secondary hypertension should also be considered in cases of a sudden worsening of hypertension, poor BP response to drug treatment or severe target organ damage, which is out of proportion to the duration and severity of hypertension. In these cases, specific diagnostic tests are indicated ( Table 2 ).

Table 2 -

Possible causes

Clinical indications

Diagnostics

Clinical history

Physical examination

Laboratory investigations

First-line test(s)

Additional confirmatory test(s)

Common causes

Renal parenchymal disease

● History of urinary tract infection or obstruction, haematuria (blood in the urine), analgesic abuse
● family history of polycystic kidney disease

Abdominal masses (in case of polycystic kidney disease)

● Presence of protein, erythrocytes, or leucocytes in the urine
● decreased GFR

Renal ultrasound

Detailed work-up for kidney disease

Renal artery stenosis

● Fibromuscular dysplasia: early onset hypertension (especially in women).
● Atherosclerotic stenosis: hypertension of abrupt onset, worsening or increasingly difficult to treat; flash pulmonary oedema

Abdominal bruit (abnormal sound)

● Difference of >1.5 cm in length between the two kidneys (renal ultrasound),
● rapid deterioration in renal function (spontaneous or in response to RAA blockers)

Renal Duplex Doppler ultrasonography

● Magnetic resonance angiography,
● spiral computed tomography
● intra-arterial digital subtraction angiography

Primary aldosteronism

● Muscle weakness
● family history of early onset hypertension and cerebrovascular events at <40 years of age

Arrhythmias (in case of severe hypokalaemia)

● Hypokalaemia (spontaneous or diuretic-induced)
● incidental discovery of adrenal masses

Aldosterone-renin ratio under standardized conditions (corrected hypokalaemia and withdrawal of drugs affecting RAA system)

● Confirmatory tests (oral sodium loading, saline infusion, fludrocortisone suppression, or captopril test)
● adrenal CT scan
● adrenal vein sampling

Uncommon causes

Pheochromocytoma

● Paroxysmal hypertension or a crisis superimposed to sustained hypertension;
● headache, sweating, palpitations and pallor;
● positive family history of pheochromocytoma

Skin stigmata of neurofibromatosis (café-au-lait spots, neurofibromas)

Incidental discovery of adrenal (or in some cases, extra-adrenal) masses

Measurement of urinary fractionated metanephrines or plasma-free metanephrines

● CT or MRI of the abdomen and pelvis;
● ¹²³I-labelled meta-iodobenzyl-guanidine scanning;
● genetic screening for pathogenic mutations

Cushing syndrome

● Rapid weight gain,
● polyuria (excessive production of urine),
● polydipsia (excessive thirst),
● psychological disturbances

Typical body habitus (central obesity, moon-face, buffalo hump, red striae (stretch marks), hirsutism)

Hyperglycaemia

24-h urinary cortisol excretion

Dexamethasone-suppression test

Box 2 -

Box 3 -

The medical history has to address the time of the first diagnosis of hypertension, current and past BP measurements and antihypertensive medications. A history of pregnancy-related hypertension is an important factor in the assessment of women with hypertension. Hypertension results in an increased risk of CVD complications, and chronic kidney disease (CKD). Thus, a careful medical history should be taken in all patients to allow for assessment of global CVD risk, with special emphasis on current and past smoking habits and evidence of dyslipidaemia and diabetes mellitus. CVD risk should be estimated using an established calculator (e.g. http://ASCVD-Risk-Estimator/). Adults at high risk for CVD have a high probability to benefit from antihypertensive drug therapy in addition to lifestyle change76.

The physical examination aims to establish the diagnosis of hypertension and screen for target organ damage and secondary causes ( box 2). The patient should sit quietly for 5 minutes before a BP reading is taken and BP cuff should be at heart level. An average of 2 to 3 BP measurements obtained at 2 to 3 separate occasions provides an accurate basis for estimation of BP77,78. At least once, BP should be measured on both arms, and differences in SBP > 20 mmHg and/or in DBP >10mmHg should initiate investigations of vascular abnormalities77. Careful attention should be paid to choosing appropriately sized cuff, particularly for the increasing number of patients with obesity. Further, BP should be measured in both sitting and standing positions to rule out orthostatic hypotension (a sudden drop of the BP when a person stands up from a lying or sitting position). This is particularly important in elderly individuals.

All patients should undergo auscultation of the carotid arteries, heart and renal arteries. Detection of murmurs (sounds audible via the stethoscope) should lead to further investigations: carotid ultrasound, echocardiography and renal ultrasound, respectively. An irregular pulse frequently indicates atrial fibrillation, which should be confirmed by an electrocardiogram (EKG). Laboratory investigations are used to detect additional risk factors, to confirm or exclude secondary hypertension, to detect clinical or subclinical target organ damage and to estimate global CVD risk ( box 3).

Prevention

The association between BP and risk of CVD highlights the importance of treating hypertension, especially when severe. Further, it also underscores the importance of strategies to reduce BP-related CVD risk in those who have a higher than normal level of BP (average systolic BP 120-129 mmHg) but below the hypertension threshold. Reducing BP in adults with a high normal BP (referred to as elevated BP in the 2017 US guidelines) provides the potential to directly reduce CVD risk and to prevent or at least slow the age-related tendency for individuals to develop hypertension.

In most countries there is a strong tendency for BP, especially systolic BP, and the prevalence of hypertension to increase progressively from childhood until late in life79. However, studies in isolated societies that have limited contact with the outside world84,85 indicate that high BP is not an inevitable consequence of aging and that the rise in BP associated with local migration by members of isolated societies is related to changes in diet, decreased physical activity and consumption of alcohol. These reports underscore the logic of efforts to prevent high BP in settings where an age-related increase in BP is common.

Lifestyle changes

A variety of nonpharmacological interventions have been shown to be effective in lowering BP and preventing hypertension. The most effective interventions are weight loss88,89,90, reduced Na⁺ intake88,89,90,91, increased potassium intake92,93, increased physical activity94, reduced consumption of alcohol95,96 and diets like the Dietary Approaches to Stop Hypertension (DASH) diet97 that combine several elements which favorably affect BP98,99 ( table 3 ). The DASH diet is especially successful when combined with other effective BP lowering interventions such as a reduced intake of dietary sodium91. Lifestyle change is the best way for the individual to implement these interventions. Even small improvements in an individual's lifestyle can be valuable. Government agency and professional society websites provide helpful tips for lifestyle change and monitoring of BP. Careful monitoring of BP is essential because the beneficial effects of lifestyle change are predicated on maintenance of the intervention100.

Table 3.

Food group

Servings*

Examples of a serving

Whole grains

6-8 per day

1 slice whole grain bread

Vegetables

4-5 per day

1 cup of raw leafy vegetables

Fruits

4-5 per day

1 medium sized fruit

Dairy products (low-fat or fat-free)

2-3 per day

1 cup of milk or yogurt

Fats and oils

2-3 per day

1 teaspoon of margarine or vegetable oil or
1 tablespoon of mayonnaise or
2 tablespoons of salad dressing

Lean meat, poultry, fish

2-3 per day

2 ounces of cooked meats, chicken or fish

Nuts, seeds and legumes

4-5 per week

1/3 cup (1.5 ounces) of nuts or
2 tablespoons of peanut butter or
2 tablespoons (0.5 ounce) of seeds or
½ cup of cooked peas or beans

Candy and added sugars

5 or less per week

1 tablespoon of sugar, jelly or jam or
1 cup of lemonade

Two complementary strategies aimed at achieving a small population-wide reduction in BP or a larger reduction in those who are at higher risk to develop hypertension can be employed to implement hypertension prevention interventions98,99,101. Modeling studies suggest that a downward shift of as little as 2 mmHg in the population distribution of diastolic BP would result in a 17% reduction in the incidence of hypertension, a 14% reduction in the risk of stroke and transient ischemic attacks, and a 6% reduction in the risk of coronary heart disease102. Public health interventions focused on dietary improvements and increases in physical activity that are known to lower BP provide the basis for the population-wide strategy. Diet in the general population can be favorably influenced by means of public health education campaigns, food product labeling, and collaborations with food manufacturers to reduce the calorie and sodium content of their products, as well as with fast food companies and restaurants to reduce portion size and to promote healthier food preparation and promotion practices. Physical activity can be enhanced by making it easier for members of the community to engage in exercise on a routine basis.

Pharmacological interventions

Low-dose pharmacological therapy has also been shown to be effective in lowering BP and preventing hypertension in three randomized controlled trials conducted in adults with high normal BP103,104,105. The Brazilian multi-center PREVER-Prevention Trial compared treatment with the low-dose long-acting thiazide-like diuretic chlorthalidone in combination with the potassium sparing agent amiloride with treatment with placebo105. Treatment with the low-dose chlorthalidone and amiloride combination resulted in both a decrement in BP and prevention of hypertension and a reduction in left ventricular mass. A drug intervention is easier to implement and maintain than a lifestyle change intervention but there is a natural reluctance to recommend a lifetime of pharmaceutical therapy for prevention of hypertension. Consideration of low-dose pharmacotherapy should be restricted to those who are at high risk of developing hypertension despite energetic efforts to lower BP by means of one or more nonpharmacological interventions105.

MANAGEMENT

BP treatment thresholds and targets

Until 2015, most guidelines recommended a target BP < 140/90 mmHg for most patients and < 150/90 mmHg for elderly patients over 60 or 80 years of age ( Table 4 )77,106. However, after the publication of the Systolic blood PRessure Intervention Trial (SPRINT)107, target systolic BP values have been frequently debated. SPRINT was a randomized, open-label controlled trial that enrolled 9361 participants without diabetes mellitus but with increased CVD risk. Patients with a history of stroke were excluded. Participants were randomized to a standard systolic BP target < 140 mmHg or intensive systolic BP target < 120 mmHg. Intensive BP treatment in SPRINT resulted in a significantly greater (25%) reduction in the primary endpoint (first occurrence of myocardial infarction, acute coronary syndrome, stroke, heart failure or death from cardiovascular causes), compared with standard treatment. Office BP measurement in SPRINT was performed with an automated device timed to start measurement after 5 minutes of rest in an effort to standardize measurements in the various clinics and minimize the white coat effect. Because large differences had been observed between automated office BP measurement and conventional auscultatory measurements (with the automated technique showing lower values)108, some groups have questioned the applicability of the SPRINT intensive systolic BP target of < 120 mmHg to ordinary office practice109. Both the appropriate method(s) of measuring office BP (automated versus manual; unattended versus attended) and the appropriate BP targets for antihypertensive treatment are currently topics of vigorous debate. In summary, newer guidelines published after the SPRINT trial generally have more aggressive goals, at least for individuals < 65 years of age ( Table 4 ).

Table 4.

Guideline

Population

Goal BP (mmHg)

Adults 65 years and older

<150/90 (<140/90 if tolerated)

Adults with diabetes, CHD or renal disease

<130/80

Adults > 80 years

< 150/90

Adults with diabetes

< 140/85

Adults with CKD without proteinuria

< 140/90

Adults with CKD with overt proteinuria

< 130/90

Adults with CHD

< 140/90

Young adults

< 130/80

Elderly > 80 years

< 150/90

Adults ≥ 60 years

< 150/90

Adults with diabetes

< 140/90

Adults with CKD

< 140/90

Adults > 80 years

SBP 140-150

Late phase elderly patients

<150/90 (<140/90 if tolerated)

Adults with diabetes or CKD

< 130/80

Adults with CHD or CVD

< 140/90

Adults ≥ 80 years

< 150

High-risk adults ≥ 50 years

≤ 120*

Adults with diabetes in whom prevention of stroke is priority

< 120

Adults with diabetes and high risk for CVD

< 130/80

Adults without additional markers of increased CVD risk

< 130/80

Older adults ≥ 65 years of age,
noninstitutionalized, ambulatory

< 130/80

Older adults ≥ 65 years of age, with comorbidities and limited life expectancy

Individualized goal based on clinical judgement and patient preference

Patient's global CVD risk and comorbidities should be considered in determining the need for pharmacologic antihypertensive treatment. The 2017 US ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults110 recommend the use of antihypertensive medication in patients with pre-existing CVD and those without a CVD event but an estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk of 10% or higher at BP levels ≥ 130/80 mmHg. In individuals without CVD and with 10-year ASCVD risk < 10%, antihypertensive medication should be initiated at BP ≥ 140/90 mmHg. ( Figure 5 ).

Non-Pharmacological Management

Lifestyle advice is recommended for all patients with hypertension. The most effective interventions are the same as for prevention of hypertension. Targeted dietary approaches can reduce the systolic BP in individuals with hypertension. For example, reducing sodium intake (ideally to <2.3 g per day, or <1.5 g per day in those most susceptible to the effects of sodium on BP, but reduction by at least 1.0 g per day is desirable) can lower the systolic BP by 2-4 mmHg (Ref). A similar reduction can be expected with increases in potassium intake to 3.5- 5.0 g per day92.

Reduced salt intake

For metabolic balance, the amount of salt consumed must be equal to that lost. Thus, under normal living conditions and physical activity levels, an intake of 5 g salt/day is considered sufficient, in line with the WHO recommendation (< 5 g per day)113. By contrast, the currently estimated dietary intake of salt is about 9-12 g per day in most countries. The current recommendations of the American Heart Association114 and American Society of Hypertension115 are stricter than the European guidelines, recommending lowering salt intake to 3.8 g per day, whereas the 2013 ESH/ESC guidelines recommend 5-6 g of salt per day77.

There is strong evidence to support population-wide recommendations to lower salt intake119,120. As more than 75% of dietary salt comes from processed foods (in western countries), any population strategy to reduce salt intake must involve food manufacturers and restaurants, in order to progressively reduce salt added to foods. So far, only three countries (Japan, Finland and the United Kingdom) have successfully reduced population salt intake121.

Moderate alcohol consumption

Keeping alcohol intake ≤2 standard drinks (~3.5 alcohol units) per day for men and ≤1 standard drink (~1.75 alcohol units) per day for women can also contribute to a 2-4 mmHg BP reduction. 95,96

Physical activity

Regular physical activity reduces BP in individuals with hypertension. Endurance training reduces BP more in persons with hypertension than in individuals with normal BP. A narrative review of 27 randomized clinical trials in individuals with hypertension showed that regular medium-intensity to high-intensity aerobic activity reduced BP by a mean of 11/5 mmHg125. Sessions lasting 40-60 minutes performed at least three times a week had the greatest effect on BP. Three randomized controlled trials of isometric exercise (strength training) showed a BP reduction of similar magnitude to that induced by aerobic exercise in individuals with hypertension125. A meta-analysis of 64 controlled studies of the efficacy of dynamic resistance training as stand-alone antihypertensive therapy showed BP reductions comparable with or greater than those with aerobic exercise training126. Greater BP reductions occurred in individuals with higher resting BP (approx. 6/5 mmHg for individuals with hypertension and 3/3 mmHg for individuals with pre-hypertension) and in non-white individuals126.

Weight Loss

Excess adiposity generally raises BP in susceptible individuals, and patients with hypertension who also have obesity require more antihypertensive medications to control their BP and are more likely to be treatment resistant127. In a recent meta-analysis, any reduction in body weight lowered systolic BP by on average 2.69 mmHg and in diastolic BP by on average 1.34 mmHg (Ref128). However, the response varies substantially between individuals. Lifestyle interventions, including hypocaloric diets and physical exercise, are commonly recommended for patients with obesity and hypertension, yet average weight loss is modest and most patients regain weight129 ( box 4).

Box 4

Weight loss is recommended for individuals with obesity, and may be particularly important if these patients also have hypertension. Medications have been developed for the treatment of obesity, but their approval status differs between the United States and Europe: some drugs are only approved in the United States (for example, lorcaserin and topiramate/phentermine), whereas others are approved in Europe only. BP reductions in patients with hypertension have been reported for some weight loss medications201, but their specific pharmacological actions may attenuate the positive influences of weight loss on BP and CVD outcomes133. Bariatric surgery is very effective in reducing body weight, and the risk for arterial hypertension is substantially reduced up to five years following bariatric surgery202. However, large and sustained body weight reductions are needed to substantially reduce BP following bariatric surgery203 and there are no large clinical trials specifically testing the effects of weight loss medications or bariatric surgery on hypertension control.

Antihypertensive Pharmacotherapy

Antihypertensive pharmacotherapy has evolved over several decades driven by development of various antihypertensive medication classes and large-scale outcomes trials proving their benefits on CVD morbidity and mortality130. Clinicians are now faced with a plethora of antihypertensive medications of different drug classes and a variety of fixed dose combinations. Typically, antihypertensive pharmacotherapy begins with first-line antihypertensive medications either in monotherapy or in combination131. Combination therapy may be preferable in patients with higher levels of pretreatment BP. First-line antihypertensive medications include ACE inhibitors, angiotensin II receptor blockers (also known as sartans), dihydropyridine calcium channel blockers, and thiazide diuretics106. Beta-blockers are also indicated in patients with heart failure and reduced left ventricular ejection fraction or post myocardial infarction, and some guidelines recommend beta-blockers as first line antihypertensive medications 77,132. The choice should be based on individual efficacy and tolerability. Ethnicity affects the response to antihypertensive medications, and it has been suggested that calcium channel blockers and diuretics may be the first choice in blacks. Further, in specific clinical situations, for example hypertension in pregnant women, other medications such as alpha-methyldopa (an agonist of alpha adrenoreceptors in the central nervous system that inhibits the sympathetic nervous system) or labetalol (a beta adrenoreceptor blocker) are preferable, whereas some first line antihypertensives, for example ACE inhibitors and angiotensin II receptor blockers, are contraindicated because of increased risk for renal teratogenicity. Divided dosing of antihypertensive drugs tends to decrease adherence and should be avoided when possible135.

BP cannot be controlled with monotherapy in many patients, particularly those with severe hypertension. When combining antihypertensive medications, it is important to consider whether the drugs have additive effects on BP or adverse effects, and whether the patient has comorbidities that mandate particular drug choices77. ACE inhibitors or angiotensin II receptor blockers, thiazide diuretics and dihydropyridine calcium channel blockers are additive in lowering BP and can be combined as double or triple combination therapies. By contrast, combining ACE inhibitors and angiotensin II receptor blockers adds little BP lowering while increasing the risk for renal dysfunction and hyperkalemia (high blood potassium levels, which can lead to cardiac arrhythmias). Similarly, combining RAAS inhibitors with beta-adrenoreceptor blockers adds little BP reduction, but this combination is indicated in patients following acute myocardial infarction or heart failure with reduced left ventricular ejection fraction for reasons beyond BP reduction.

Dihydropyridine calcium channel blockers.

Dihydropyridine calcium channel blockers elicit vasodilation by blocking vascular smooth muscle L-type calcium channels. They are effective antihypertensive drugs with extensive experience in large clinical trials136. A practical advantage of this drug class is that it can be combined with all other first-line antihypertensives. Peripheral edema, which is explained by peripheral arterial vasodilation rather than worsening heart failure or kidney dysfunction, is a common side effect, particularly in individuals with obesity. Non-dihydropyridine calcium channel blockers, especially verapamil, also inhibit cardiac calcium channels, which can reduce heart rate and cardiac contractility141. Calcium channel blockers can induce or worsen constipation, especially in institutionalized older persons142. All calcium channel blockers modestly inhibit the drug metabolizing enzyme cytochrome P450 3A4, and, therefore, could elicit important drug-interactions143.

Thiazide-type and thiazide-like diuretics.

Thiazide-type diuretics (for example, hydrochlorothiazide) have a benzothiadiazine ring, whereas thiazide-like diuretics (for example, chlorthalidone, metolazone and indapamide) lack the benzothiadiazine structure. Both subclasses of thiazide diuretics inhibit Na⁺ and CI⁻ co-transporters in renal tubules, thereby promoting natriuresis, and have been an important component of pharmacological hypertension management ever since the first trials showing morbidity benefits of antihypertensive therapy144. Over the years, diuretic doses have been substantially reduced to attain better risk-benefit profiles. Thiazide-type and thiazide-like diuretics can worsen glucose metabolism increasing the risk for new onset diabetes mellitus, but whether or not this metabolic action translates into long-term increases in CVD risk has been called into question145. Hydrochlorothiazide, the most commonly prescribed thiazide-type diuretic worldwide, may be less effective in mitigating CVD risk compared to chlorthalidone or indapamide146,147. Drug-related electrolyte disturbances, including hypokalemia and hyponatremia (low blood potassium and sodium levels, respectively), are particularly important adverse effects; hypokalemia can lead to cardiac arrhythmias and muscle weakness, and hyponatremia can cause confusion, seizures and coma. The risk for hypokalemia is reduced when thiazide-type and thiazide-like diuretics are combined with potassium supplements or potassium-sparing agents, such as ACE inhibitors, angiotensin receptor blockers, or potassium-sparing diuretics. Hyponatremia is a potentially life threatening adverse effect, particularly in elderly persons.

Beta-adrenoreceptor blockers.

Beta-adrenoreceptor blockers lower BP reducing cardiac output, heart rate, renin release and adrenergic control nervous system effects148. They improve outcomes following acute myocardial infarction and in patients with heart failure with reduced left ventricular ejection fraction, but, in the absence of these comorbidities, beta-adrenoreceptor blockers are inferior to other first line antihypertensives in reducing CVD morbidity and mortality149. This effect has been attributed to lesser reductions in aortic BP150 and adverse effects on body weight151 and glucose metabolism with beta-adrenoreceptor blockade. Some of these disadvantages might be mitigated with newer vasodilator beta-adrenoreceptor blockers, such as nebivolol and carvedilol152. However, there are no large-scale antihypertensive trials demonstrating that this difference translates into better clinical outcomes. Beta-adrenoreceptor blockers may promote bronchial obstruction is patients with asthma and should not be combined with non-dihydropyridine calcium channel blockers such as verapamil that lower sinus node rate or atrioventricular conduction.

Treatment Resistant Hypertension

Treatment resistant hypertension is commonly diagnosed when office BP is >140/90 mmHg despite treatment with three or more properly dosed antihypertensive drugs including a diuretic and secondary hypertension has been ruled out159. Poor treatment adherence is a common cause of apparent treatment resistant hypertension. The true prevalence of treatment resistant hypertension is unknown, but an estimated 12.8% of all individuals with hypertension in the United States and 15.3 % of those treated with antihypertensives fulfill the criteria for treatment resistant hypertension160. Adding a fourth or fifth drug could lead to satisfactory BP control in these patients. The PATHWAY trial rotated patients with treatment resistant hypertension through different add on drugs or placebo in a randomized fashion161. All patients received a standardized antihypertensive regimen comprising three drugs, including a diuretic. Compared with alpha-adrenoreceptor or beta-adrenoreceptor blockade, the mineralocorticoid receptor antagonist spironolactone was the most effective fourth antihypertensive drug. In another study in patients whose BP was uncontrolled despite receiving three drugs, sequential addition of a mineralocorticoid receptor antagonist followed by a loop diuretic (which acts at the ascending limb of the loop of Henle in the kidney) was more effective than adding an ACE inhibitor followed by a beta-adrenoreceptor blocker162. Overall, mineralocorticoid receptor antagonism is a reasonable choice in patients with difficult to control hypertension. Given the risk of inducing hyperkalemia163, serum potassium concentrations should be monitored.

Device-based Treatments

Device-based treatments have been primarily developed for patients with severe resistant hypertension whose BP cannot be controlled with antihypertensive drugs156. Catheter-based renal nerve ablation164,165, electrical carotid sinus stimulation166,167, modulation of baroreflex transduction with a dedicated carotid stent168, carotid body denervation169, and deep brain stimulation170 are thought to lower BP through SNS inhibition. Creation of a defined arteriovenous stent with a coupler device lowers BP by reducing peripheral vascular resistance171. These treatments are in various stages of clinical development, with the most extensive data available on renal nerve ablation and electrical carotid sinus stimulation. None has yet been proven efficacious in lowering BP in randomized sham-controlled clinical trials164,161,167, because either the primary endpoint was not achieved or no trials have been conducted. Finally, trials with hard clinical endpoints do not exist.

QUALITY OF LIFE

Health-related quality of life (HRQoL) is a multi-dimensional concept that includes domains related to physical, mental, emotional, and social functioning; studies demonstrate that each additional disease, as well as the severity of these diseases, is associated with declines in HRQOL 172. Population-based studies have consistently shown that being diagnosed with hypertension is associated with worsening of HRQoL even after adjusting for other comorbidities173,174. Altered HRQoL in persons with hypertension has been attributed to a variety of factors, including the diagnosis, treatment, and effects of alterations (both elevations and reductions) in BP173.

Antihypertensive medication use is associated with a variety of symptoms that could lower HRQoL177. Observational studies showed an association between the number of antihypertensive medications prescribed and worsening of the HRQoL178. Some classes of antihypertensive medications, (for example, ACE inhibitors) are better tolerated than others (for example, beta blockers and centrally acting agents, such as alpha-methyldopa) and result in significantly better scores on measures of general well-being179. Further, small differences in HRQoL have even been reported among medications of the same class, e.g., enalapril vs. captopril180. However, clinical trials with newer antihypertensive agents have generally indicated that they are extremely well-tolerated and can enhance the effects of non-pharmacological treatment on HRQoL177,181. In the Treatment of Mild Hypertension Study (TOMHS), combining lifestyle modifications with any of five different antihypertensive medication classes resulted in greater improvements in HRQoL than lifestyle modifications plus placebo181.

Treatment-related reductions in BP could have a negative effect on HRQoL, particularly in older and more frail patients at high risk of hypotension. Clinical trials performed in the 1990s that evaluated patients with very high baseline BP, for example, the Systolic Hypertension in the Elderly Program Trial (SHEP) and the Systolic Hypertension in Europe Trial (Syst-Eur), generally found minimal effects of BP reductions on HRQoL182,183. Two more recent clinical trials have targeted lower BPs (intensive systolic BP target < 120 mmHg versus standard systolic BP target < 140 mmHg ), it had been postulated that this lower BP might be expected to cause cerebral hypoperfusion, resulting in falls, dizziness, and cognitive impairment184,185,107. In a substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, HRQoL was evaluated in 1,028 participants randomized to either intensive or standard therapy. No differences in mental function were noted between treatment groups, but intensive therapy was associated with a small, not clinically significant, decrease in physical function185. In the Systolic Blood Pressure Intervention Trial (SPRINT), targeting systolic BP <120 mmHg required 1 additional antihypertensive medication compared to standard treatment to target systolic BP < 140 mmHg and was generally safe and well tolerated107,186. Compared to standard treatment, intensive treatment did not affect the perceived HRQOL of SPRINT participants, measured by patient reported outcomes of physical and mental health, self-reported satisfaction with care and medication adherence, even when stratifying on age and comorbidities186. Almost 90% of participants in both treatment groups reported satisfaction with their BP care, and more than 1/3 described improvement in satisfaction over baseline levels.

Quality of life concerns remain an important aspect of hypertension management. SPRINT has demonstrated that with careful clinical management, lower BP can be targeted without concern of worsening physical and mental function. Clinicians must seek the optimal balance of reducing CVD morbidity and mortality while maximizing well-being for each individual patient.

OUTLOOK

Overall, prevention will probably contribute least to any improvement in BP-associated disease burden. This is because 80% of the world is in the process of developing, which hitherto has inevitably been associated with increased exposure to the main environmental determinants of raised BP such as excess intake of calories, alcohol and salt. Food and drink industries, governments and education systems would be required to cooperate in order to reverse this pattern

Implementation of preventive strategies has largely been limited to high income countries. Despite reasonably compelling evidence to the contrary111, recommendations that the general population should restrict salt intake have been questioned on the basis of largely suboptimal observational data189. Such confusion worsens an already very difficult public health challenge. Data show that only approximately half of people with hypertension are aware of their condition190, and the Lancet Commission on hypertension identified improving awareness of hypertension is a critical action needed to improve the current disease burden191,192. The global BP awareness campaign promoted by the International Society of Hypertension whereby World Hypertension Day was extended to become May Measurement Month (MMM) in 2017 could contribute substantially to improving rates of routine BP screening around the world83. Over 1.20 million adults (≥18 years) from >100 countries were screened as part of MMM and the ensuing data allied to health-economic analyses will be used to persuade policy makers in each country that enhanced local BP screening and treatment facilities are wise financial investments.

Meanwhile, single-pill formulations of the drug combinations most commonly recommended in current guidelines (calcium channel blocker plus a diuretic, calcium channel blocker plus a RAAS-blocker or diuretic plus a RAAS-blocker) are readily available and have low production costs. In addition, a 3-drug combination of a calcium channel blocker, a diuretic and a RAAS-blocker132 should also be produced for more severe hypertension, with low dose spironolactone available as a fourth-line agent161. Hence, 1 or 2 tablets will be able to control BPs of all but a small proportion of patients with hypertension.

These formulations should be made available and affordable in all countries of the world.191 Additional local obstacles to the distribution and delivery of these agents to patients with hypertension within each country will also have to be overcome - among which the lack of effective screening programmes is crucial191.

Antihypertensive medications are prescribed by different health professionals in different countries. However, even in high income countries, much of the "routine" uncomplicated hypertension management could, and probably should be carried out by nurse practitioners or other non-physician health workers. In more remote parts of the world, the use of e-healthcare techniques196 should be increasingly used to facilitate task-shifting or task sharing by non-physician health-workers where doctors are unavailable197.

In summary, although there are many interesting unanswered scientific research questions in the field of hypertension ( Box 5), perhaps the most pressing need to reduce the diseas burden is to evaluate the best way(s), at a local level, to screen routinely for raised BP and then to deliver the best, most affordable, evidence-based combination of antihypertensive agents. Meanwhile, efforts to drive public health policy towards encouraging more healthy diets and lifestyles from a BP and CVD viewpoint should be encouraged and basic scientific research that might allow precision medicine to be applied to patients with hypertension must also continue.

Box 5

Measurement Issues

Is hypertension management improved by basing treatment strategies on serial unattended office BP measurements, out of office (home or ambulatory) BP measurements or central BP measurements?

How should BP be measured in patients with atrial fibrillation?

Treatment Issues

Should salt restriction at the population level continue to be recommended at current targets?

To what extent should age, estimated CVD risk and concomitant conditions influence treatment thresholds?

Should white-coat hypertension be treated?

If management strategy is to be influenced by central or out of office BP levels, what treatment thresholds and targets should be used?

Should reducing 24-hour and longer-term BP variability be a consideration in the selection of drug treatment for optimal CVD protection?

What combinations of antihypertensive agents give optimal CVD protection, stratified by age and ethnicity?

What is the optimal BP treatment target stratified by age, CVD risk and concomitant disease status?

What is the optimal management of treatment resistant hypertension that is resistant to 4 agents including spironolactone?

If treatment thresholds are to be driven by estimated CVD risk, at what level should antihypertensive drug treatment be initiated and what other CVD protective agents should be considered?

Is initiating drug therapy with 2 hypertensive agents more effective than initiating with monotherapy for optimal CVD prevention?

Acknowledgments

P.K.W. was supported by P20GM109036 (Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases) from the National Institute of General Medical Sciences.

Footnotes

Competing interests

G.B. served as Consultant for Janssen, Bayer, AbbVie, Vascular Dynamics, Relypsa and Merck; served/serves as Principal Investigator for FIDELIO trial (Bayer), Steering Committee member (CREDENCE)-Janssen, SONAR-AbbVie, and CALM-2-Vascular Dynamics. J.J. served as consultant for Novartis, Novo-Nordisc, Boehringer-Ingelheim, Sanofi, Orexigen, Riemser, Theravance, Vivus; and is cofounder of Eternygen GmbH. S.O. (in the previous 24 months) has received research grant support or reimbursement for travel to meetings or other, non-financial support from Actelion Clinical Research/George Clinical; AstraZeneca AB; Bayer; Lundbeck; Novartis; Novo Nordisk; Rox Medical; has consulted for Actelion/George Clinical, Lundbeck, Novo Nordisk and ROX Medical; served as Director/Principal Investigator, SPRINT University of Alabama at Birmingham (UAB) Clinical Center Network (CCN); and sub-investigator UAB CCN clinical site; for which Takeda and Arbor Pharmaceuticals donated 5% of medication used. N.R.P. served as advisory board member (ad hoc) for Pfizer, Takeda, MSD, Servier, and Medtronic (companies producing blood pressure lowering agents/devices); received speaker honoraria from Servier, AstraZeneca, Napi Labs, and Menarini; received research funding from Servier, Pfizer and Menarini; and is the President of the International Society of Hypertension. George Health Enterprises, the social enterprise arm of The George Institute for Global Health, has applied for a patent in the area of low-dose combinations on which A.R. is listed as an inventor; and has received investment to develop fixed-dose combinations containing aspirin, statin and BP lowering drugs. AR is an investigator on grants for several trials of blood pressure lowering interventions. G.G. has received lectures fees from Merck and Astra Zeneca. M.C.A., R.C., A.F.D., D.R.B. and P.K.W. declare no competing interests.

How to cite this Primer

Publisher's note

References

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# data[].attributes.attachment_link.description
Systemic arterial hypertension is the most important modifiable risk factor for all-cause morbidity and mortality worldwide and is associated with increased risk of cardiovascular disease (CVD). Fewer than half of those with hypertension are aware of ...

# data[].attributes.body
Se realizaron análisis de subgrupos y metarregresión para explorar la fuente de heterogeneidad. El protocolo del estudio ha sido registrado con PROSPERO, número CRD42019147330. En total, 52 artículos incluidos en el metanálisis con un total de 54 estudios. Se identificó un aumento evidente en la prevalencia de presión arterial alta mediante la aplicación de nuevos criterios diagnósticos. La prevalencia agrupada de presión arterial alta entre la población fue del 53,01% (intervalo de confianza del 95%: 51,13-54,88%). El análisis de subgrupos mostró que la región, el país y la edad de la OMS podrían influir significativamente en la prevalencia de hipertensión (P < 0,01). Los análisis de metarregresión revelaron que la calidad de los estudios y la proporción de sexos (hombres, %) no contribuyeron a la heterogeneidad de los resultados (P > 0,05)

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Affiliations

¹ Zhanggong District Center for Disease Control and Prevention, Ganzhou, 341000, Jiangxi, PR China. 975839312@qq.com.

² Shantou University Medical College, Shantou, 515000, Guangdong, PR China. 842592361@qq.com.

³ Shenzhen Cancer Hospital, Shenzhen, 518000, Guangdong, PR China.

⁴ Ganzhou People's Hospital, Ganzhou, 341000, Jiangxi, PR China.

Affiliations

¹ Zhanggong District Center for Disease Control and Prevention, Ganzhou, 341000, Jiangxi, PR China. 975839312@qq.com.

² Shantou University Medical College, Shantou, 515000, Guangdong, PR China. 842592361@qq.com.

³ Shenzhen Cancer Hospital, Shenzhen, 518000, Guangdong, PR China.

⁴ Ganzhou People's Hospital, Ganzhou, 341000, Jiangxi, PR China.

Abstract

To understand the prevalence of high blood pressure among the general adult population under the new diagnostic criteria. PubMed and Embase databases were systematically searched. Two investigators independently performed data extraction and quality assessment, and the disagreements were resolved by consensus with a third investigator. The random-effects model was performed to pool the prevalence of high blood pressure among the population. Subgroup and meta-regression analyses were performed to explore the source of heterogeneity. The study protocol has been registered with PROSPERO, number CRD42019147330. In total, 52 articles included in the meta-analysis with a total of 54 studies. An obvious increase in the prevalence of high blood pressure was identified by the application of new diagnostic criteria. The pooled prevalence of high blood pressure among the population was 53.01% (95% confidence interval 51.13-54.88%). Subgroup analysis showed that the WHO region, national, and age could significantly influence the prevalence of hypertension (P < 0.01). Meta-regression analyses revealed that study quality and sex ratio (male, %) did not contribute to the heterogeneity of the results (P > 0.05). The sensitivity analysis showed that the results were stable. With the use of new diagnostic criteria, the prevalence of high blood pressure has shown an upward trend, especially in Europe countries. Prevention and control measures should focus more on improving cardiovascular and cerebrovascular status in Europe countries. Standard electronic blood pressure monitors were recommended for use in future studies, and at least two more readings should be taken during a visit.

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national center for biotechnology information

# data[].attributes.attachment_link.title
Prevalence of high blood pressure under 2017 ACC/AHA guidelines: a systematic review and meta-analysis - PubMed

# data[].attributes.attachment_link.description
To understand the prevalence of high blood pressure among the general adult population under the new diagnostic criteria. PubMed and Embase databases were systematically searched. Two investigators independently performed data extraction and quality assessment, and the disagreements were resolved by ...

# data[].attributes.body
La hipertensión arterial (HTA), se debe en su mayoría a una causa identificable (Menor del 5% del total de los casos de hipertensión arterial; cuya remoción o corrección desencadenada un control óptimo de la presión arterial y el muchos casos la curación de la enfermedad.
Entre ellas destacan: enfermedades renales, endocrinas, misceláneas y medicamentos tales como: Anticonceptivo hormonales, corticosteroides, agentes vasoconstrictores, simpaticomiméticos, antidepresivos tricíclicos, inhibidores de la monoaminoxidasa,  anfetaminas, antiinflamatorios no esteroideo (AINES), ciclosporina, eritropoyetina entre otros.

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Factores de riesgo

·         Sexo masculino

·         Edad (♂ ≥ 55 años; ♀ ≥ 65 años)
·         Fumar (ahora o en el pasado)
·         Dislipidemia

·         Colesterol total >190 mg/dL y/o

·         HDL-colesterol ♂ <40 mg/dL; ♀ <46 mg/dL y/o

·         Glucosa en sangre en ayunas 102–125 mg/dL

·         Hiperuricemia

·         Obesidad

·         Índice de masa corporal (IMC) ≥ 30 kg/m² y/o

·         Obesidad abdominal (circunferencia de la cintura ♂ ≥ 102 cm; ♀ ≥ 88 cm)

·         Antecedentes familiares de inicio temprano de hipertensión arterial

·         Sedentarismo

·         Factores psicosociales y socioeconómicos

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Continuing Medical Education

Abstract

The World Health Organization estimates that 54% of strokes and 47% of cases of ischemic heart disease are the direct consequence of high blood pressure, which thus takes its place among the main risk factors for cardiovascular morbidity and mortality ( 1). The declining incidence of stroke in recent decades is accounted for in large measure by the reduction of blood pressure ( 2). Even though the epidemiological association between high blood pressure and cardiovascular morbidity and mortality is well known, and despite the fact that sufficient evidence exists to justify antihypertensive treatment ( 3), blood pressure is often not adequately controlled. Either the blood pressure is not measured, or the physician fails to react in the face of elevated blood pressure values ( 4), or treatment is not provided optimally, or the patient fails to take the necessary medication regularly ( 5). In patients who suffer from treatment-resistant arterial hypertension, the blood pressure cannot be adequately controlled even if the patient does take the prescribed medication regularly. In patients with essential hypertension, none of the currently available clinical methods can detect a specific cause of the elevated blood pressure. Causes of secondary hypertension such as renal artery stenosis, hyperaldosteronism, or pheochromocytoma, must be considered in the differential diagnosis, particularly in younger patients and those whose blood pressure is hard to control. Secondary types of hypertension call for specific diagnostic and therapeutic approaches (e.g., a pheochromocytoma must be resected) and will not be discussed here. In what follows, we provide an overview of the epidemiology and pathophysiology of essential arterial hypertension and derive recommendations for the treatment of the affected patients.
Learning objectives
This article should enable the reader to

diagnose arterial hypertension and treat this leading cardiovascular risk factor,

be familiar with the definition of blood pressure target values for treatment, and

know how to treat patients in conformity with the current guidelines.

Methods

A selective search for original articles and reviews was carried out in PubMed with special attention to current guidelines and meta-analyses, which are given here as references. This article is also based on the authors' scientific and clinical experience.
Epidemiology
In the 1990s, the prevalence of arterial hypertension in Germany was still higher than the mean value among other Western countries. German epidemiological data from the years 2008-2011 reveal a decline in the frequency of uncontrolled hypertension from 22% to 13% in women and from 24% to 18% in men () ( 6). Meanwhile, however, the prevalence among men aged 18 to 29 rose from 4.1% to 8.5%.

Pathophysiology

Elevated blood pressure must be due to elevated cardiac output, elevated peripheral vascular resistance, or a combination of both. Each of these mechanisms is regulated, in turn, by hemodynamic, neural, humoral, and renal processes, all of which vary in their contribution from one individual to another (). As persons grow older, the predominant cause of hypertension tends to be elevated peripheral vascular resistance, often in combination with increased stiffness of the vessels, which manifests itself clinically as isolated systolic hypertension ( 7). Familial clustering implies a genetic predisposition whose interaction with environmental factors, such as the intake of salt and calories and the degree of physical exercise, ultimately determines how severe the rise of blood pressure will be.

Diagnostic evaluation and screening

In their current, updated joint guidelines on the diagnosis and treatment of arterial hypertension ( 8), the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) retain the threshold value of = 140/90 mm Hg for the definition of high blood pressure when measured in a doctor's office. At least three measurements should be made on each of several days, with 1-2 minutes between measurements and with a 3-5 minute pause before blood pressure is measured with the patient sitting. The optimal conditions for blood pressure measurement should be maintained ( box 1). Measurements from the arm in patients with an arm circumference of 22-32 cm are made with a standard cuff (12-13 cm wide, 35 cm long); for larger upper arms, cuffs that are 15-18 cm wide are available. When the blood pressure is first measured, it should be measured on both sides. If the difference in the values obtained on the two sides is >20 mmHg systolic or >10 mmHg diastolic, the following potential causes must be ruled out, and, if the blood pressure is lower on the left side, the possibility of an aortic isthmus stenosis should be considered:

BOX 1

The bladder should be emptied before measurement.

The patient should not consume coffee, alcohol, or tobacco for at least one hour before the measurement.

The patient should be seated for 3-5 minutes before the measurement in quiet surroundings at a pleasant temperature.

Measurement in a relaxed, seated position, with backrest.

The patient's arm should be free of clothing.

The legs should be planted on the floor, not crossed.

The arm should be relaxed and should rest on a firm surface during the measurement.

Cuff size suitable for arm circumference.

The site of the measurement should be at heart level.

At least 2 measurements should be taken 1-2 minutes apart. The patient should remain quietly seated without moving or talking.

Aortic arch syndrome due to atherosclerosis, or, rarely, vasculitis;

Unilateral subclavian artery stenosis;

Aortic dissection.

Further measurements are subsequently always made on the arm with the higher values. Orthostatic hypotension is defined as a fall in blood pressure by more than 20 mmHg systolic and/or more than 10 mmHg diastolic after the patient has been standing for three minutes ( 9). If orthostatic hypotension is suspected, particularly in an elderly or diabetic patient, two further measurements should be made 1 and 3 minutes later, with the patient still standing.

The diagnosis should be confirmed by a 24-hour ambulatory measurement or by automated home blood pressure measurements. The values obtained by these methods are usually lower than those obtained in the doctor's office. This fact is taken into account by the lower recommended cutoff values ( 8). A 24-hour ambulatory measurement is also particularly helpful for ascertaining the presence of white-coat hypertension or of masked hypertension.

Orthostatic hypotension is defined as a fall in blood pressure by more than 20 mmHg systolic and/or more than 10 mmHg diastolic after the patient has been standing for three minutes ( 9).

A patient with white-coat hypertension regularly has an elevated blood pressure in the doctor's office, but normal values when measured at home. The prevalence of this phenomenon in the general population is approximately 13% ( 10). The long-term risk of cardiovascular events may be slightly higher in persons with white-coat hypertension than in persons without it ( 11).

In contrast, masked hypertension is the situation in which the measured blood pressure values are normal in the doctor's office, but elevated at home. It is more common in young people, males, smokers, overweight or diabetic persons, and those suffering from anxiety or stress ( 12). The incidence of cardiovascular events in persons with masked hypertension is similar to that of persons with persistently elevated blood pressure ( 13).

10-15% of persons with hypertension have secondary hypertension due to a potentially treatable cause. If the history and basic diagnostic assessment suggest this possibility ( box 2), a targeted supplementary evaluation should be performed (). The patient should be asked about his or her intake of substances that elevate blood pressure, including licorice, amphetamines, cocaine, oral contraceptive drugs, mineralo- and glucocorticoids, nonsteroidal anti-inflammatory drugs, erythropoietin, and cyclosporine. Anticancer drugs, particularly angiogenesis inhibitors and tyrosine kinase inhibitors, can also elevate blood pressure.

BOX 2

Evidence from the basic diagnostic work-up

Severe and, especially, malignant hypertension

Intractability

Persistent blood pressure elevation after a long period of good blood pressure control

Hypertension of sudden onset

Lack of a nocturnal drop in blood pressure ("non-dipper") or even a nocturnal rise in blood pressure ("reverse dipper") in the 24-hour long-term measurement

Unusual age of onset (before age 30 or after age 60)

Table 1

Hyperaldosteronism

1.4 -10%

Laboratory testing
Aldosterone-renin quotient and absolute
serum aldosterone concentration

* Sodium chloride tolerance test
* CT or MRI of the adrenal glands
* Selective adrenal venous sampling

Cushing syndrome

0.5%

Cortisol in 24-hour urine sample

Dexamethasone suppression test

Pheochromocytoma

0.2 - 0.5%

Metanephrines in plasma

* CT or MRI of the abdomen
* ¹²³ I-MIBG scintigraphy

Thyroid diseases

1- 2%

Measurement of serum TSH, fT ₃, and fT ₄

Thyroid ultrasonography or scintigraphy

Renal parenchymal diseases

1.6 - 8%

Renal ultrasonography
Urinalysis

Detailed work-up for renal disease

Renal artery stenosis

1- 8%

Duplex ultrasonography of the kidneysand renal arteries

Contrast-enhanced CT or MRI of the renal arteries

Sleep apnea

>5 -15%

Polygraphy

Polysomnography

Aortic isthmus stenosis

<1%

Blood pressure difference right vs. left arm and upper vs. lower limb
Echocardiography

Contrast-enhanced CT or MRI of the thoracic aorta

High blood pressure is usually accompanied by other cardiovascular risk factors that further potentiate the risk. It follows that an evaluation of the patient's overall risk should always be the first objective ( box 3).

BOX 3

* modified from ( 8), eGFR, estimated glomerular filtration rate

According to the current recommendation, the higher the patient's overall cardiovascular risk, the more strictly the blood pressure should be controlled and the earlier drug treatment should be initiated () ( 8). Moreover, before any treatment is given, the potential causes of secondary hypertension should be excluded (). The possibility of pseudoresistance to treatment due to white-coat hypertension or suboptimal drug compliance should be borne in mind. Compliance can be checked by blood pressure measurement after supervised drug intake, or else by measurement of the active substance(s) in the patient's serum or urine. These factors are too often left out of consideration, even by specialists ( 14). In one study, out of 731 patients carrying the diagnosis of treatment-resistant hypertension, 26.5% actually had either pseudoresistant essential hypertension or a secondary type of hypertension. In 47% of cases, blood pressure became normal after a suitable change in the drug regimen ( 14).

Treatment

Target values for blood pressure

According to the update of the European ESH/ESC guidelines (2018), all patients, including those with renal failure or diabetes, should have their blood pressure reduced to less than 140/90 mmHg (as measured in the doctor's office) at the beginning of their treatment ( 8). Most patients will tolerate this well; for those who do, a further reduction of blood pressure is recommended. A target blood pressure range is defined, including a lower limit ( 8). For patients aged 18-65, a target systolic blood pressure below 130 mmHg, but no less than 120 mmHg is suggested. The same holds for diabetic patients, whereas the recommendation for patients with renal failure is a somewhat higher target systolic blood pressure range (below 140 mmHg, but no less than 130 mmHg). For patients over age 65, the recommended target systolic blood pressure range is also below 140 mmHg, but no less than 130 mmHg. The target diastolic blood pressure range for all patients, regardless of age, is below 80 mmHg, but no less than 70 mmHg. In elderly patients in particular, attention must be paid to side effects, and the blood pressure target may have to be reset. The available scientific evidence on the treatment of high blood pressure in the elderly is limited, because the elderly are often excluded from clinical trials ( 15).

The German High Blood Pressure League recommends the reduction of blood pressure to less than 135/85 mmHg only in patients who have a high cardiovascular risk ( 16), stating that the advantage of low systolic blood pressure has not yet been demonstrated for hypertensive patients who suffer from diabetes mellitus, have already sustained a stroke, or are physically handicapped or dependent on nursing care.

The U.S. American cardiological societies, in the most recent update of their guidelines, classify blood pressure values in the range of 130-139/85-89 mmHg as grade I hypertension, but state that this should initially be treated without drugs in most cases () ( 17, 18). In the updated European guidelines, this is designated as the upper range of normal blood pressure, and it is recommended that drug treatment be considered for patients with blood pressure in this range only if their cardiovascular risk is very high () ( 8). More liberal cutoff values for high blood pressure are set by the United Kingdom's National Institute for Health and Care Excellence (NICE) ( 19), which defines hypertension as an initial measurement = 140/90 mm Hg with subsequent measurements = 135/85 mm Hg ().

The association of blood pressure with the occurrence of cardiovascular events in patients at high risk can be depicted by a J-shaped curve: over-aggressive blood pressure reduction (to <120 mmHg systolic or <70 mmHg diastolic) only causes more side effects without any further reduction of cardiovascular events ( 20). On the other hand, the findings of the Systolic Pressure Intervention Trial (SPRINT) contributed to a downward trend in blood pressure cutoff values in the U.S. American and European guidelines. In this trial, 9361 patients over age 50 with a high cardiovascular risk, but without diabetes mellitus, were randomized to systolic blood pressure reduction to either <120 mmHg or <140 mm Hg ( 21). Over a mean follow-up time of 3.26 years, the patients with the lower blood pressure target had a lower incidence of a combined cardiovascular endpoint (hazard ratio [HR]: 0.75, 95% confidence interval: [0.64; 0.89]) and a lower risk of death from a cardiovascular cause (HR: 0.57 [0.38; 0.85]. The patients with the lower blood pressure target achieved a mean systolic blood pressure of 121 mmHg over a three-year period by taking a mean of 2.8 antihypertensive drugs, while those with the lower target achieved a mean systolic blood pressure of 134 mmHg by taking a mean of 1.8 antihypertensive drugs. The automated blood-pressure measurements in this trial were carried out after a five-minute rest period and without medical supervision, resulting in values that were a mean of 12.7/12.0 mmHg lower than those obtained in a conventional doctor's office setting ( 22). It follows that these findings are not directly applicable to routine outpatient care.

A somewhat different picture arose from a Cochrane Review concerning the question whether a reduction of blood pressure by 9.5/4.9 mmHg (down to = 135/85 mmHg from starting values of 140-160/90-100 mmHg) might lower morbidity and mortality in patients already suffering from cardiovascular disease ( 23). Data derived from 9795 subjects, including data from SPRINT, were evaluated; no difference was seen either in overall mortality (relative risk [RR] 1.05 [0.90; 1.22]) or in cardiovascular mortality (RR 0.96 [0.77; 1.21]). Lower blood pressure did, however, lead to a 1.6% absolute risk reduction for fatal and non-fatal cardiovascular events. A further meta-analysis concerned the effects of reducing blood pressure from 150-160/95-105 mmHg to <140/90 mmHg in elderly patients with a mean age of 75 years ( 24). A total of 8221 patients from three different trials were included in this meta-analysis, with SPRINT patients excluded for methodological reasons. There was no statistically significant effect on overall mortality, stroke, or serious cardiovascular events. Overall, it was concluded that there is an individual, relatively narrow blood pressure corridor that can be recommended for each patient on the basis of his or her age, comorbidities, and ability to tolerate the treatment. It remains to be seen whether this concept can be practically applied in routine clinical situations.

Non-pharmacological treatment

The two pillars of antihypertensive treatment are non-pharmacological treatment and drug treatment (). Lifestyle changes are always to be considered first as a means of lowering blood pressure ( 8), and it makes sense to maintain these changes even after the later initiation of drug treatment. The most important measures are a low-salt diet, adequate potassium intake, avoidance of excessive alcohol consumption, smoking cessation, a healthy, balanced diet, physical exercise, and weight loss.

In a meta-analysis, the reduction of salt intake from 201 mmol/day (a fairly typical value for the German population) to 66 mmol/day lowered blood pressure by a mean of 5.5/2.9 mmHg in white hypertensive patients ( 25). The effect is variable, however: not every patient benefits from a low-salt diet. Some antihypertensive drugs, particularly inhibitors of the renin-angiotensin-aldosterone system, tend to be more effective if the patient is on a low-salt diet ( 26). According to the ESH/ESC guidelines, daily salt intake should not exceed 5 g ( 8). Potassium intake can be increased by increased consumption of vegetables and fruit.

In randomized controlled trials, regular endurance training lowered blood pressure by a mean of 11/5 mmHg ( 27, 28). The strongest effect was found in patients who exercised during 40- to 60-minute periods at least three times per week. A meta-analysis revealed that regular dynamic strength training can also positively affect blood pressure ( 29, 30).

Overweight and obese persons are at higher risk for arterial hypertension, need more antihypertensive medication, and are more commonly resistant to treatment than patients with normal weight ( 31, 32). It is currently recommended that all persons should have a body-mass index between 20 and 25 kg/m ², with a waist circumference less than 94 cm in men and 80 cm in women ( 14). The value of weight-reducing drugs for obese hypertensive patients is unclear ( 33, 34). The massive weight reduction brought about by bariatric surgery is associated with an initial marked improvement in blood pressure ( 35). Over the long term, however, this effect seems to diminish, and persistent weight reduction by at least 10 kg is needed to lower systolic blood pressure by 6 mmHg [-10.66; -1.38 mmHg] ( 36).

Antihypertensive pharmacotherapy

Drug treatment can be initiated with a single drug or a combined preparation ( 13, 37). The ESC and ESH, in their updated joint guideline, recommend that most patients should take two antihypertensive drugs at the start of pharmacotherapy, preferably combined in a single tablet ( 8). The recommended first line of treatment consists of preparations that are constituted from the following four drug classes: angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor subtype 1 (AT1) blockers (sartans), long-acting calcium channel blockers of the dihydropyridine type, and thiazide-like diuretics (). Even though beta-adrenoreceptor blockers are inferior to these substance classes with respect to cardiovascular protection ( 38), they are considered a suitable component of first-line treatment in some countries. Beta-blockers are used in patients who suffer from angina pectoris, have sustained a myocardial infarction in the past, or have heart failure, or else for the control of heart rate ( 8). On the one hand, the choice of antihypertensive drug is based on individual efficacy and tolerability, for which there are still no good predictors; on the other hand, certain antihypertensive drugs improve outcomes in patients with certain underlying diseases and should, therefore, be used preferentially in these patients (). Preparations with a long half-life that can be given once per day are preferable for reasons of compliance. In view of the circadian rhythms of circulatory regulation, it may be better for patients to take long-acting antihypertensive drugs in the evening ( 39), but it remains unclear whether this has any positive effect on cardiovascular events.

ACE inhibitors and AT1 receptor antagonists have been extensively studied in large-scale clinical trials ( 40). They improve the survival of patients with heart failure and have a beneficial effect on diabetic nephropathy, and should therefore be given preferentially to patients with these conditions (). They may also lower the risk of developing type 2 diabetes mellitus ( e1). Rising creatinine values and a corresponding drop in the estimated glomerular filtration rate (eGFR) by as much as 30% after the initiation of treatment with an ACE inhibitor or an AT1 receptor antagonist are not infrequently seen, particularly in patients with diabetic nephropathy, and should not necessarily prompt the physician to discontinue these drugs. This phenomenon is due to the desired reduction of the blood pressure faced by the renal glomeruli, resulting in a functional reduction of the eGFR. AT1 receptor antagonists carry a much lower risk of inducing cough and angioedema, but their side-effect profile is similar to that of ACE inhibitors in other respects ( e2).

Calcium channel blockers of the dihydropyridine type are effective antihypertensive drugs and can, in principle, be combined with any other type of first-line antihypertensive drug. Peripheral edema due to peripheral vasodilatation is a common side effect and sometimes leads to discontinuation of the drug ( 18). In a Cochrane analysis, the incidence of peripheral edema was 38% lower when the calcium channel blocker was given in combination with an ACE inhibitor or an AT1 receptor antagonist, probably because of the relaxation of post-capillary resistance vessels brought about by the second drug ( e3). calcium channel blockers can cause or worsen constipation, particularly in elderly and immobile patients. They can also cause clinically significant drug interactions by inhibiting the enzyme cytochrome P450 3A4.

Thiazide-like diuretics have been a mainstay of antihypertensive treatment for decades ( e4). Hydrochlorothiazide is the one most commonly prescribed around the world, even though it seems to be less effective than indapamide or chlorthalidone ( e5). Electrolyte disturbances are a common side effect, especially in elderly patients ( e6); the main types are hyponatremia and hypokalemia. 4.1% of elderly hypertensive patients treated with chlorthalidone had a serum sodium concentration below 130 mmol/L ( e7). The risk of hypokalemia is lower when a thiazide diuretic is given in combination with an ACE inhibitor, an AT1 receptor antagonist, or a potassium-sparing diuretic.

Beta-blockers are inferior to other first-line antihypertensive drugs for the reduction of blood pressure ( 13, e8). They can cause weight gain ( e9). Non-vasodilating beta-blockers have a deleterious effect on glucose metabolism ( e10). Beta-blockers may worsen bronchoconstriction in patients with asthma. Nor should they be combined with verapamil or diltiazem, two drugs that can slow the sinus rhythm or prolong atrioventricular conduction. Beta-blockers do improve the prognosis of patients who have sustained an acute myocardial infarction and/or suffer from chronic congestive heart failure, and they are, therefore, indicated for patients with these conditions, independently of their antihypertensive effect ( 8).

ACE inhibitors and AT1 receptor antagonists are contraindicated during pregnancy. Pregnant women may take older antihypertensive drugs such as dihydralazine and alpha-methyldopa; they may also take beta-blockers, such as metoprolol, and extended-release nifedipine. Dihydralazine and nifedipine, however, should not be given during the first trimester ( e11).

Treatment-resistant hypertension

Even when all of these measures are taken, some 10% of hypertensive patients treated in routine clinical practice do not achieve adequate blood pressure control ( e12, e13). The definition of treatment-resistant hypertension is blood pressure that persistently remains over 140/90 mmHg despite treatment with three antihypertensive drugs in optimal doses, one of which is a diuretic. The definition also requires the exclusion of potential causes of secondary hypertension. Treatment-resistant hypertension often turns out to be treatable once the matter of patient compliance and the potential for further improvement of the drug regimen have been properly addressed; in our experience, the true prevalence of treatment-resistant hypertension is closer to 4-5%. In these patients, the therapeutic spectrum must be widened in order to counteract the still unaltered, high cardiovascular risk.

The treatment should be directed against two main pathophysiological mechanisms: overactivity of the sympathetic nervous system and volume excess due to excessive sodium retention, renal failure, or an excessively high aldosterone level. Hypervolemia can be countered with high-dose diuretics or with supplementary treatment with a mineralocorticoid-receptor antagonist. This was confirmed in the Pathway 2 trial ( e14): 285 hypertensive patients whose mean blood pressure, measured in the doctor's office, was 157/90 mmHg under standard treatment with an ACE inhibitor or AT1 blocker, a calcium antagonist, and a diuretic at the highest tolerated doses were given either spironolactone (25-50 mg), doxazosine (4-8 mg), bisoprolol (5-10 mg), or placebo for a period of 12 weeks in a double-blind crossover trial. If tolerated, the dose was doubled at 6 weeks. Absolute reduction of blood pressure was most pronounced with spironolactone (values of -12.8 mm Hg, -8.7 mm Hg, -8.3 mm Hg, and -4.1 mmHg, respectively). Blood pressure became normal under this treatment in 58% of patients. The frequency of serious side effects and the treatment discontinuation rate did not differ among treatment groups. Elevated activity of the sympathetic nervous system ( e15) also provides the rationale for some of the interventional techniques that have been developed for this group of patients.

Conclusion

The treatment of arterial hypertension with a combination of lifestyle interventions and drugs can markedly lower cardiovascular risk. In most patients, blood pressure can be lowered effectively with first-line antihypertensive drugs, but monotherapy often does not suffice. With regard to blood pressure target values, many questions remain open. We expect that the newly altered target values will give rise to a lively discussion of their advantages and potential risks in the very near future.

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Question 1 Question 2 Question 3 Question 4 Question 5 Question 6 Question 7 Question 8 Question 9 Question 10
Acknowledgments

Translated from the original German by Ethan Taub, M.D.

Footnotes
Conflict of interest statement
Prof. Jordan has served as a paid scientific consultant for Bayer, Eternygen, Johnson & Johnson, Novartis, Novo-Nordisk, and Theravance. He is a co-founder of Eternygen GmbH.

Prof. Reuter has received lecture fees from, and has served as a paid consultant for, Bayer, Cordis, CVRx, Medtronic, and Servier.

Prof. Kurschat states that he shas no conflict of interest.

References

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Arterial Hypertension: Diagnosis and Treatment

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Continuing Medical Education The World Health Organization estimates that 54% of strokes and 47% of cases of ischemic heart disease are the direct consequence of high blood pressure, which thus takes its place among the main risk factors for cardiovascular morbidity and mortality ( 1).

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Se obtuvo 14 256 encuestas en 26 ciudades del Perú, localizadas en la costa, sierra y selva. En la sierra, las ciudades están situadas a diferentes alturas sobre el nivel del mar.El 50,8% de la población total correspondió a varones y 49,2% a mujeres, con un promedio de edad de 43,5 años para varones y 40,7 años para mujeres. En Perú, la prevalencia de la HTA es del 23,7% al 27,3% del total de la población; 27,3% a 31,6% en la zona costera, de 20,4% a 23,2% en la región andina, y de 22,7% a 26,6% en la parte amazónica, estas cifras para ambos sexos en personas mayores de 18 años

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Similares en SciELO

SIMPOSIO: HIPERTENSIÓN ARTERIAL

Epidemiología de la Hipertensión Arterial en el Perú
Epidemiology of Arterial Hypertension in Peru
1 Médico Cardiólogo. Profesor Emérito, Universidad Peruana Cayetano Heredia. Ex Presidente de la Sociedad Peruana de Cardiología

Objetivos: Determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en el Perú. Diseño, lugar, participantes: Aplicación de encuesta y medida de presión arterial a población adulta de ambos sexos, mayores de 18 años en 26 ciudades, 10 en la costa, 4 en la selva y 12 en la sierra, localizadas a diferentes alturas a nivel del mar. En la sierra, fueron agrupadas por su altitud en menos y más de 3000 msnm. En total, quedaron 14 256 encuestas válidas. Intervenciones: La obtención de la muestra se realizó entre febrero y noviembre de 2004. La presión arterial fue obtenida con los mismos tensiómetros, de acuerdo a las recomendaciones establecidas. Para el diagnóstico de la presión arterial, se utilizó el criterio del VII Comité Nacional Conjunto. Resultados: La prevalencia de hipertensión en la población general fue 23,7% (varones 13,4% y mujeres 10,3%). En la costa, la prevalencia fue 27,3%; en la sierra 18,8% y 22,1% en las altitudes menores y mayores de 3000 msnm, respectivamente; en la selva, 22,7%. A partir de la cuarta década de la vida, la posibilidad de desarrollar hipertensión fue mayor en la costa que en las otras regiones. Los hipertensos diastólicos fueron predominantes en la sierra, sobre los 3 000 msnm; 55% de la población no sabía que era hipertenso; de quienes recibían tratamiento, solo 45,1% estaba compensado; la mayoría (82,2%) recibía tratamiento con los inhibidores de la enzima convertidora de la angiotensina (ECA) I. Se especula teorías en relación al hematocrito, vasodilatación e hipervascularización. Conclusiones: La hipertensión es casi similar en las tres regiones del Perú. A partir de la cuarta década de la vida, la posibilidad de desarrollar hipertensión es mayor en la costa. Los hipertensos diastólicos fueron predominantes en la sierra, sobre los 3 000 msnm; más de la mitad de la población no sabía que era hipertenso y, de quienes recibían tratamiento, solo 45,1% estaba compensado; la gran mayoría recibía tratamiento con los inhibidores específicos de la enzima convertidora de la angiotensina (ECA) I.

PALABRAS CLAVES: Hipertensión arterial, epidemiología, Perú, diagnóstico, costa, sierra, selva.

Objective: To determine arterial hypertension prevalence, knowledge, treatment, and control, in Peru. Design, setting, participants: Cross sectional survey application and blood pressure measurement performed in 26 cities in 18 year-old or over adult population, 10 cities in the coast, 12 in the mountains at different altitude (below and above 3 000 meters above sea level), and 4 in the jungle. Interventions: The study done between February and November 2004 considered valid 14 256 surveys. Blood pressure was obtained with the same standard equipment, and diagnosis followed the recommendations of the Joint National Committee's Seventh Report. Results: Arterial hypertension prevalence was 23,7% (males, 13,4%; females, 10,3%). In the coast, the prevalence was 27,3%; in the mountains, 18,8% below 3 000 meters and 22,1% above 3 000 meters; in the jungle, 22,7%. After the fourth decade of life the possibility of developing hipertensión was higher in the coast than in the other regions of Peru. Diastolic hypertension was predominant above 3 000 meters. The study determined that 55% of the population did not know they had hypertension; from those under treatment, 45,1% were compensated; 82% received angiotensin converting enzyme I inhibitors. We speculate on hematocrit, vasodilation and hypervascularization theories. Conclusions: Hypertension prevalence was similar in the three Peruvian regions. The possibility of developing hypertension after the fourth decade of life was higher in the coast. Diastolic hypertension was predominant above 3 000 meters. Over one half of the population did not know they had hypertension; from those Ander treatment 45,1% were compensated; most of the patients received angiotensin converting enzyme I inhibitors.

Keywords: Arterial hypertension, epidemiology, Peru, diagnosis

La hipertensión arterial es uno de los factores de riesgo modificable de mayor prevalencia en el mundo. Participa en el desarrollo de la enfermedad aterosclerótica cardiovascular, en la morbimortalidad por eventos cardiacos, cerebrovasculares, insuficiencia renal y enfermedad vascular periférica, como riesgo continuo sin evidencia de umbral, hasta por debajo de 115/75 mmHg, por lo que la expectativa de vida de estos pacientes se encuentra reducida1.

La epidemiología de la hipertensión arterial en el Perú ha sido preocupación permanente de los investigadores peruanos, los que han realizado múltiples estudios en las distintas ciudades del país, con resultados variados, diferentes e inconsistentes, por haberse realizado en lugares y en grupos poblacionales distintos, aplicando metodología y criterios de definición diversos.

La hipertensión arterial ha sufrido cambios en su definición, de acuerdo a los sucesivos Reportes del Comité Nacional Conjunto, tanto en Estados Unidos como en Europa, criterios que son aplicados en la mayoría de los estudios epidemiológicos del mundo.

El Perú es un país geográficamente accidentado, con sus tres regiones costa, sierra y selva. En la sierra, las ciudades están situadas a diferentes alturas sobre el nivel del mar. En cada región, las costumbres de trabajo, alimentación, educación y cultura son diferentes, lo que influye en los factores de riesgo cardiovascular y probablemente en el desarrollo de la aterosclerosis.

Al componente socio cultural y al incremento de la población habría que agregar los cambios biológicos por la altura y la predisposición genética.

En el Perú, en las últimas décadas han acontecido importantes cambios en la distribución de la población, con un incremento acelerado, básicamente por una gran migración del campo a la ciudad, de la región andina a la costa, de rural y agrícola a grandes concentraciones urbanas, en busca de mejores niveles de vida.

La hipertensión arterial disminuye la calidad de vida y la supervivencia de la población, por lo que es un reto importante para la salud pública. Para un tratamiento adecuado, es necesario determinar la prevalencia, el tratamiento y control de la hipertensión arterial en las diferentes ciudades en las 3 regiones del país, lo que permitirá conocer la realidad nacional y poder aplicar la prevención, método importante y económico difundido en todo el mundo, responsabilidad que pertenece a los organismos de Salud Pública del Estado.

Presentamos los resultados del estudio de la prevalencia de la hipertensión arterial en el Perú realizado de febrero a noviembre de 2004, en 26 ciudades del país, distribuidas en costa, sierra y selva.

Para la recolección de los datos, se utilizó el protocolo diseñado para determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en la población adulta de ambos sexos, mayores de 18 años, en 26 ciudades del país, 10 ciudades en la costa, 12 en la sierra y 4 en la selva. En la sierra, las ciudades están localizadas a diferentes alturas sobre el nivel del mar. La obtención de la muestra se realizó de febrero a noviembre de 2004. Se realizó 14 826 encuestas en las 26 ciudades; se excluyó del análisis 538 encuestas, vueltas a realizar en la ciudad del Callao y que fueron utilizadas como control de calidad. Además, se excluyó 32 encuestas, por presentar datos inconclusos o recogidos inadecuadamente, quedando 14 256 encuestas válidas. La presión arterial fue obtenida utilizando los mismos 19 tensiómetros de mercurio calibrados en Lima y luego transportados por las monitoras, enfermeras licenciadas en investigación, a las diversas ciudades, de acuerdo con un cronograma previamente determinado. En cada ciudad, se nombró un investigador principal, miembro de la Filial de la Sociedad Peruana de Cardiología y, en los lugares donde no había filial, se nombró un médico de la ciudad de reconocido prestigio. Los investigadores principales fueron reunidos en Lima en dos etapas, con los que se realizó seminarios-talleres para unificar criterios, la forma de obtener los datos, llenar las encuestas y el método adecuado de la toma de la presión arterial, ilustrados con videos que fueron proporcionados para las sedes respectivas.

Cada investigador, en su sede, nombró a los investigadores secundarios y a las encuestadoras, que podían ser médicos, estudiantes de medicina y enfermeras, todos calificados y con experiencia. El día previo a la encuesta, la monitora reunía y entrenaba a los participantes en la obtención de los datos y la toma de la presión arterial. Las encuestas fueron realizadas en lugares públicos, parques y otros lugares concurridos, alejados de los hospitales, centros de salud y postas médicas. La presión arterial fue obtenida al final de la encuesta, mientras la persona permanecía sentada y en reposo, en el miembro superior derecho, de acuerdo a las recomendaciones del Sétimo Comité Nacional Conjunto ². Las encuestas originales quedaron archivadas en la ciudad del lugar de la obtención y la copia en la Oficina Central de la Sociedad Peruana de Cardiología. Después de depurar los datos obtenidos, se realizó los cálculos estadísticos de la prevalencia de la población total del Perú, por ciudades aisladas y luego las ciudades por región natural, costa, sierra y selva. Luego, las ciudades de la sierra fueron agrupadas por su altitud, en menos y más de 3 000 msnm, consideradas medianas y grandes alturas, respectivamente.

Para el diagnóstico de la presión arterial, se utilizó el mismo criterio del Sétimo Comité Nacional Conjunto (2004), que considera normal < 120/80 mmHg; prehipertensión, < 139/89 mmHg; hipertensión arterial grado I > 140/90 mmHg y grado II, > 160/90 mmHg. Se consideró también hipertensas a las personas que tenían diagnóstico previo por un profesional médico y personas que tenían tratamiento para hipertensión arterial. Se consideró control farmacológico de la hipertensión arterial cuando con el tratamiento hipotensor se encontró presión arterial sistólica menor de 140 mm de Hg y diastólica menor de 90 mm de Hg.

Se obtuvo 14 256 encuestas en 26 ciudades del Perú, localizadas en la costa, sierra y selva. En la sierra, las ciudades están situadas a diferentes alturas sobre el nivel del mar.

El 50,8% de la población total correspondió a varones y 49,2% a mujeres, con un promedio de edad de 43,5 años para varones y 40,7 años para mujeres. En el análisis de la distribución de la población, se encuentra la mayoría de los encuestados en las primeras décadas de la vida, para disminuir progresivamente hacia las últimas décadas, con hallazgo similar en ambos sexos y en las tres regiones del país ( Tabla 1).

La prevalencia de la hipertensión arterial en la población general del Perú fue de 23,7%, en mayores de 18 años, lo que correspondería a 3 650 000 habitantes, estimado en base al censo 2005, con un predominio de hipertensos varones de 13,4% sobre hipertensas mujeres de 10,3%. Predominio de sexo masculino que persiste en los hipertensos de la costa, sierra y selva.

La prevalencia de la hipertensión arterial por sexo, de toda la población, fue 27,1% en varones y 20,4% en mujeres ( Tabla 2).

En toda la población y en las tres regiones, la prevalencia de la hipertensión arterial se incrementó progresivamente con la edad en ambos sexos, con predominio de la costa hasta la década de los sesenta, cuando aparecieron algunos cambios. En la sierra, dicha prevalencia declinó y aumentó en la selva, con relación a la costa. Estos resultados indicarían que, la probabilidad de desarrollar hipertensión arterial a partir de la cuarta década de vida, siempre es mayor en la costa que en la selva y menor aún en la sierra, a iguales edades, por influencia de probables factores que discutiremos posteriormente. ( Figura 1)

La hipertensión arterial sistólica es predominante en las primeras décadas de la vida, para luego decaer progresivamente, un comportamiento diferente al de las hipertensiones diastólica y sistodiastólica. Figura 2.

La prevalencia de la hipertensión arterial en la costa fue 27,3%, en la sierra 20,4% y en la selva 22,7%. En la sierra, al separar las ciudades cuya altura era por debajo de 3 000 msnm (metros sobre el nivel del mar) la prevalencia fue 18,8%, en las ciudades de menor altura, y sobre 3 000 msnm, la prevalencia fue mayor, 22,1%, hallazgo de gran importancia, que será analizado en la discusión. En las cuatro regiones, hay predominio del sexo masculino ( Figura 3).

Las ciudades con mayor y menor prevalencia en el país fueron: el Callao, con 34,5%, y Abancay, con 12,4%, respectivamente, como se observa en la figura 4, en ella se dispone las ciudades en relación a las tres regiones del país.

En todas las ciudades, la hipertensión arterial fue de mayor prevalencia en el sexo masculino; excepto en Chachapoyas, Cajamarca, Cerro de Pasco y el Callao, donde este predominio no es significativo.

La prevalencia de la hipertensión arterial en las ciudades de la altura no mostró una relación directa de mayor altitud a menor prevalencia de la hipertensión arterial; los resultados fueron variables. Las ciudades de la sierra con mayor prevalencia fueron Chachapoyas, Arequipa, Huaraz y Puno y, las de menor prevalencia, Huánuco y Abancay, ciudades situadas en la sierra, por debajo de los 3 000 msnm. Figura 4.

Analizando los resultados del VII Report, que define presión normal o ideal, prehipertensión, hipertensión estadio I y estadio II. En toda la población, la hipertensión arterial estadio I (17,9%) fue de mayor prevalencia que el estadio II (5,8%), que es de mayor severidad y con predominio del sexo masculino en ambos estadios. La presión arterial normal y la prehipertensión (considerados normales) fueron siempre de mayor prevalencia en las mujeres y hombres respectivamente ( Tabla 3).

Con relación a la altura sobre el nivel del mar, la presión arterial normal (ideal) fue siempre de mayor presentación en la sierra 'media' (49,7%) y 'alta' (45,3%) y en la selva (44,4%), en comparación a los resultados de la costa (37,1%). Mientras que, el estadio prehipertensión fue de presentación similar en las cuatro regiones del país.

La prevalencia en ambos estadios I y II fue siempre menor en la sierra y selva, en comparación a la costa. Un hallazgo importante fue encontrar que la prevalencia de la hipertensión arterial en las ciudades con altitud sobre 3000 msnm es ligeramente mayor que la prevalencia de las ciudades de altura por debajo de 3000 msnm ( Figura 5).

Los hipertensos diastólicos fueron siempre predominantes en la sierra situada sobre los 3 000 msnm. Figura 6.

Analizando la distribución de los hipertensos de acuerdo al "conocimiento de su condición de hipertensos, tratamiento y control" se encuentra que del total de la población de hipertensos 55,1% no sabían que eran hipertensos, y quienes sí conocían su condición de hipertensos fueron 44,9%.

De los que conocían que eran hipertensos, 72,7% recibía diferente tratamiento, 18,9% farmacológico, 4,6% dietético, 9,2% tratamiento farmacológico y dietético y 12,2% ningún tratamiento. Lo más saltante de quienes recibían tratamiento, solo 45,1% estaban compensados y la mayoría, 54,9%, era hipertenso no compensado. Esto demuestra la ineficacia del tratamiento que se presenta en ambos sexos y en las tres regiones del país en donde el 64,6% de los hombres y 42,6% de las mujeres ignoraban su condición de hipertensos. En el análisis de las tres regiones, el mayor desconocimiento fue en la sierra (59,9%), luego en la selva (57%) y en la Costa (51%). El desconocimiento de su hipertensión arterial fue siempre mayor en los hombres en la sierra y selva, mientras que en la costa el desconocimiento fue similar tanto en hombres como en mujeres ( Figura 7).

Los resultados del tratamiento farmacológico que recibían los hipertensos muestran que la gran mayoría (82,2%) recibía inhibidores de la enzima convertidora, seguidos por los calcioantagonistas dihidropiridínicos (12%) y luego otros hipotensores. ( Tabla 4).

Este esquema terapéutico se repite en las tres regiones del país.

Esta encuesta representa el estudio epidemiológico más grande sobre la prevalencia de la hipertensión arterial (HTA) y de otros factores de riesgo cardiovascular realizados en el Perú. Comprende 26 ciudades de las tres regiones de país: costa, sierra y selva. Las ciudades de la sierra se encuentran situadas a diferentes alturas sobre el nivel del mar. La preparación previa del personal médico y paramédico para la obtención de los datos de la encuesta y la toma de la presión arterial de acuerdo a la buena practica clínica, el uso de los mismos tensiómetros de mercurio en todas las ciudades, permitió tener datos más exactos y precisos sobre la detección, tratamiento y control de la hipertensión arterial en la población general. El análisis de la distribución por edad y sexo, de la población encuestada, fue similar en todas las regiones del Perú. La mayor población corresponde a las primeras décadas de la vida y luego disminuye progresivamente hasta las últimas décadas, lo que indica la obtención adecuada de la muestra.

Los datos obtenidos de este estudio deben ser tomados en forma relativa, al comararlos con estudios epidemiológicos nacionales e internacionales previos; los que fueron realizados utilizando diferentes variables y el empleo de diferentes definiciones de hipertensión arterial3-35.

En el presente estudio, se utilizó los criterios del VII Comité Nacional Conjunto del 20042.
De acuerdo a los resultados, 23,7% de la población mayor de 18 años en el Perú, tiene hipertensión arterial, que representa alrededor de 3 650 000 habitantes, población basada en el último censo de 2004. En las tres regiones del país, se encontró una mayor prevalencia de hipertensos en el sexo masculino (13,4%) sobre el sexo femenino (10,3%), lo que está de acuerdo con estudios nacionales previos.

La prevalencia promedio de la HTA en mayores de 60 años fue 48%, lo que representa un alto porcentaje de la población. Además, la prevalencia de la HTA se incrementó a medida que avanzaba la edad, en toda la población, siendo mayor en la costa sobre los 60 años de edad, en comparación con las otras regiones del país. Esto nos lleva a considerar que, la probabilidad de desarrollar hipertensión arterial es mayor en la costa que en la sierra y selva, a edades equivalentes, lo que podría estar en relación con el estrés, la alimentación, el modo de trabajo y el sedentarismo, es decir el modo de vida en las grandes ciudades, independientemente de la herencia y la genética.

La prevalencia de la hipertensión arterial es mayor en la costa (27,3%) que en la selva (22,7%) y la sierra (20,4%). El análisis de los resultados en la sierra demuestra que hay una mayor prevalencia en las ciudades situadas a mayor altura, sobre 3 000 msnm (22,1%), cuando se compara con las ciudades localizadas por debajo de los 3 000 msnm (18,8%).

Estos resultados de la altura contrasta con lo que se había establecido que, en la sierra la prevalencia de la hipertensión arterial era menor cuando la altura era mayor. Este concepto fue basado en los resultados de diferentes investigadores peruanos, destacando las investigaciones de Ruiz y col, realizadas en Milpo, un asiento minero a 4 100 msnm8,9, 18, 28, en el cual encontraron una menor prevalencia usando otra definición de HTA. Otros autores, como Lorena, en el Cusco (3 400 msnm) y en el Valle Sagrado de los Incas (2 700 msnm) señala una prevalencia de 10% y 3%, respectivamente, en 197913, y Mispireta, en Tarma (2 900 msnm), una prevalencia de 6%, en 198022.

Hay que señalar que estos estudios epidemiológicos fueron realizados en pequeñas poblaciones, algunos en asientos mineros, y con diferentes definiciones del HTA. En la actualidad, hay una serie de factores importantes en el aspecto socioeconómico, demográfico y epidemiológico en las tres regiones del país, que contribuyen a explicar estos cambios, tales como el incremento de la población en las ciudades por la migración del campo a la ciudad, lo que trae la urbanización, con cambios en el estilo de vida, como la alimentación, el sedentarismo y la industrialización, que conlleva el incremento del estrés. Se argumentó la posibilidad de la influencia racial para explicar esta menor prevalencia, ya que la población en las grandes alturas tiene un predominio de raza mestiza, con una minoría blanca y negra y de escasa raza amarilla.

En las ciudades de la selva, encontramos una prevalencia de 22,7%, lo que contrasta con resultados anteriores, que señalaban una prevalencia de 5%, debido a los mismos factores señalados anteriormente22.

La prevalencia de la HTA en las distintas ciudades del Perú no tiene un patrón de presentación y no existe una correlación entre el tamaño de la población, la altura de las ciudades, en relación con el nivel del mar y la selva. Así, el Callao, puerto principal en la costa del Perú, es la ciudad con mayor prevalencia (34,5%) y no es la ciudad más poblada. Por otro lado, Abancay, situada a 2 300 msnm, es la ciudad con menor prevalencia (12,4%); y, Cerro de Pasco, situada a mayor altura, tiene 17,7% de prevalencia. El análisis de los resultados de la HTA, cuando se aplica la definición del VII Comité Nacional Conjunto (2004), demuestra una mayor prevalencia de normotensos (presión ideal), en la sierra y selva, en comparación a la costa, que tiene un comportamiento opuesto a la prevalencia de la hipertensión estadio I y II, siendo mayor en la costa que en la sierra y selva.

En la sierra, las ciudades situadas sobre los 3 000 msnm tiene una mayor prevalencia que en las ciudades de la sierra situadas a menor altura, debajo de los 3 000 msnm, debido a los mismos cambios de modo de vida señalados anteriormente. La distribución de los hipertensos, en sistólicos, diastólicos y sistodiastólicos, demuestra que los hipertensos diastólicos aislados son los de más prevalencia en las tres regiones del Perú, siendo mayor en la sierra.

Se postuló la existencia de una relación 'directa-parcial' significativa entre hematocrito y presión arterial diastólica, especulando que la policitemia existente en los habitantes de la altura, que es el resultado de la hipoxia crónica, compensaría la disminución de la presión diastólica producida por vasodilatación e hipervascularización, incrementando el área de la sección transversal y disminuyendo la resistencia periférica al flujo, lo que llevaría a disminuir la presión arterial sistémica; ello da como resultado que las cifras de la presión arterial diastólica sean similares a las del nivel del mar. Esta compensación fisiológica explicaría por qué la presión arterial diastólica es mayor en habitantes de la sierra que viven a un nivel mayor de 3 000 msnm, donde este mecanismo compensatorio no estaría presente, debido a una mayor policitemia. Así mismo, este mecanismo compensatorio explicaría por qué la prevalencia de la hipertensión diastólica es más alta en los habitantes de mayor edad, que tienen una mayor rigidez de los vasos, a diferencia de los adultos jóvenes, donde la hipervascularidad sanguínea estaría compensada por una mayor elasticidad de las paredes arteriales, disminuyendo la resistencia periférica al flujo, que al final disminuye la presión arterial sistémica36.

Solo 44,9% de la población total de hipertensos tenía conocimiento de su condición de hipertensos. De estos hipertensos, 27,3% no recibía ningún tipo de tratamiento; y, de los 72,7% que recibía algún tratamiento, solo prácticamente la mitad de ellos (45,1%) estaba compensado con tratamiento médico y/o farmacológico.

En conclusión, del total de hipertensos solo 14,7% estaba adecuadamente controlado, porcentaje muy bajo y que debe ser tomado en cuenta por las instituciones de salud del Estado, en colaboración con las sociedades médicas, que deben realizar campañas de difusión a nivel nacional.

Los resultados del tratamiento farmacológico que recibían los hipertensos, muestran que la gran mayoría (82,2%) recibía inhibidores de la enzima convertidora (ECA), seguidos por los calcioantagonistas dihidropiridínicos (12%) y luego otros hipotensores, lo que podría estar en relación con el costo de la medicina.

Los datos epidemiológicos son obtenidos del Estudio sobre factores de riesgo cardiovascular por los doctores Luis Segura y Régulo Agusti, y en colaboración con múltiples investigadores nacionales y auspiciado por la Sociedad Peruana de Cardiología.

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CORRESPONDENCIA

Dr. Régulo Agusti C.

ragustic1@terrra.com.pe

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Epidemiología de la Hipertensión Arterial en el Perú

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Citado por SciELO Similares en SciELO SIMPOSIO: HIPERTENSIÓN ARTERIAL Epidemiología de la Hipertensión Arterial en el Perú Epidemiology of Arterial Hypertension in Peru 1 Médico Cardiólogo. Profesor Emérito, Universidad Peruana Cayetano Heredia. Ex Presidente de la Sociedad Peruana de Cardiología Objetivos: Determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en el Perú.

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Factores de riesgo:
- Edad  (Hombres ≥ 55 años; Mujeres ≥ 65 años ). Este factor es debido al endurecimiento progresivo de la vasculatura arterial, es decir, cambios lentos en el colágeno vascular y aumento de la aterosclerosis.
- Factores inmunológicos: Enfermedades infecciosas y reumatológicas (artritis reumatoidea)

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Nat Rev Dis Primers. Author manuscript; available in PMC 2019 Apr 23.

Published in final edited form as:

Suzanne Oparil, ¹ Maria Czarina Acelajado, ² George L. Bakris, ³ Dan R. Berlowitz, 4, ⁵ Renata Cífková, ⁶ Anna F. Dominiczak, ⁷ Guido Grassi, 8, ⁹ Jens Jordan, ¹⁰ Neil R. Poulter, ¹¹ Anthony Rodgers, ¹² and Paul K. Whelton ¹³

Abstract

Systemic arterial hypertension is the most important modifiable risk factor for all-cause morbidity and mortality worldwide and is associated with increased risk of cardiovascular disease (CVD). Fewer than half of those with hypertension are aware of their condition, and many others are aware but not treated or inadequately treated, although successful treatment of hypertension reduces the global burden of disease and mortality. The aetiology of hypertension involves the complex interplay of environmental and pathophysiological factors that affect multiple systems, as well as genetic predisposition. Evaluation of patients with hypertension includes accurate standardized blood pressure (BP) measurement, assessing patients' predicted risk of atherosclerotic CVD, evidence of target organ damage, detection of secondary causes of hypertension and presence of comorbidities, including CVD and kidney disease. Lifestyle changes, including dietary modifications and increased physical activity, are effective in lowering BP and preventing hypertension and its CVD sequelae. Pharmacological therapy is very effective in lowering BP and preventing CVD outcomes in most patients; first line antihypertensive medications include angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers, dihydropyridine calcium channel blockers and thiazide diuretics.

INTRODUCTION

Systemic arterial hypertension (hereafter referred to as hypertension) is characterized by persistently high blood pressure (BP) in the systemic arteries. BP is commonly expressed as the ratio of the systolic BP (that is, the pressure that the blood exerts on the arterial walls when the heart contracts) and the diastolic BP (the pressure when the heart relaxes). The BP thresholds that define hypertension depend on the measurement method ( Table 1 ). Several aetiologies can underlie hypertension. The majority (90-95%) of patients have a highly heterogeneous 'essential' or primary hypertension with a multifactorial gene-environment aetiology. A positive family history is a frequent occurrence in patients with hypertension, with the heritability (a measure of how much of the variation in a trait is due to variation in genetic factors) estimated between 35% and 50% in the majority of studies1,2. Genome-wide association studies (GWAS) have identified ~120 loci that are associated with BP regulation and together explain 3.5% of the trait variance3,4,5. These findings are becoming increasingly important as we search for new pathways and new biomarkers to develop more-modern 'omics'-driven diagnostic and therapeutic modalities for hypertension in the era of precision medicine6.

Table 1 -

Category

Subtype

Systolic BP (mmHg)

Diastolic BP (mmHg)

Office BP

NA

≥ 140

≥ 90

Ambulatory BP

Daytime (awake)

≥ 135

≥ 85

Night time (asleep)

≥ 120

≥ 70

24hr

≥ 130

≥ 80

Home BP

NA

≥ 135

≥ 85

Several rare, monogenic forms of hypertension have been described (for example, the Liddle syndrome, glucocorticoid-remediable aldosteronism (a mineralocorticoid excess state) and mutations in PDE3A (which encodes cGMP-inhibited 3',5'-cyclic phosphodiesterase A)), in which a single gene mutation fully explains the pathogenesis of hypertension and indicates the best treatment modality7,8,9. If hypertension is caused by another condition (for example, primary aldosteronism, pheochromocytoma (a neuroendocrine tumour of the adrenal glands or other neuroendocrine tissues) or renal artery stenosis), it is referred to as secondary hypertension.

Hypertension is the most common preventable risk factor for cardiovascular disease (CVD; including coronary heart disease, heart failure, stroke, myocardial infarction, atrial fibrillation and peripheral artery disease), chronic kidney disease (CKD) and cognitive impairment, and is the leading single contributor to all-cause death and disability worldwide10. The relationship between BP and the increased risk of CVD is graded and continuous, starting as low as 115/75 mmHg, well within what is considered to be the normotensive range. Successful prevention and treatment of hypertension are key in reducing disease burden and promoting longevity in the world's population. In treating hyperteinsion, it is important to consider a person's predicted atherosclerotic CVD (ASCVD) risk more than the level of BP alone, as persons with high CVD risk derive the greatest benefit from BP lowering treatment11.

This Primer will discuss the epidemiology and pathophysiology of primary hypertension, prevention strategies for slowing the progression of BP elevation, management strategies (including optimal BP targets) for lowering BP and preventing CVD outcomes in patients with established hypertension and the effects of antihypertensive treatment on quality of life; finally, we will explore knowledge gaps, future trends and the outlook for hypertension research and treatment over the next decade.

EPIDEMIOLOGY

As economic development progresses, hypertension initially affects those with a high socioeconomic status, but at later stages of economic development, the prevalence of hypertension and its consequences are greatest in those with lower socioeconomic status; this phenomenon is seen both within and between countries. Further, the speed of change prevalence of hypertension since 2000 to 2010 has been much more rapid than in previous epidemiological transitions15.

Disease burden

Globally, 3.5 billion adults now have non-optimal systolic BP levels (that is, >110-115 mmHg) and 874 million adults have systolic BP ≥140 mmHg. Thus, approximately one in four adults has hypertension16. Between 1990 and 2015 there was a 43% increase in the total global number of healthy life years lost to non-optimal BP, driven by population increase, population aging and a 10% increase in the age-standardized prevalence of hypertension16. The Global Burden of Disease study has shown that non-optimal BP continues to be the biggest single risk factor contributing to the global burden of disease and to global all-cause mortality, leading to 9.4 million deaths and 212 million lost healthy life years (8.5% of the global total) each year10.

CVD risk

Prospective observational studies have repeatedly demonstrated a strong, continuous positive relationship between BP and CVD, with no evidence of a threshold for risk throughout the usual range of BP observed in clinical practice. The relationship between BP and CVD applies to both systolic BP and diastolic BP, but is somewhat more robust for systolic BP in adults19. It is noted in both sexes, at all ages throughout adulthood and for all major manifestations of CVD, including stroke (ischaemic and haemorroagic), coronary artery disease, heart failure, peripheral vascular disease and end stage renal disease (although there are variations in the strength of the associations and the slopes of the curves)17,18,19,20 ( Figure 1 ). The relationship is independent of other CVD risk factors, and level of BP has proven to be a major component of CVD risk in all prediction models21. Approximately two-thirds of all adults who have hypertension or receive treatment with BP lowering medication at 30 years of age have a ~40 % higher risk of experiencing a CVD event than their age-matched and sex-matched counterparts with a lower level of BP18. In addition, CVD events in individuals with hypertension tend to manifest about five years earlier than in individuals with a lower level of BP18.

In individuals of 40-69 years of age, a 20 mmHg rise of systolic BP or a 10 mmHg rise of diastolic BP regardless of baseline values is associated with more than a doubling of the risk for stroke or ischaemic heart disease mortality17, whereas a systolic BP reduction of 5 mmHg can decrease stroke mortality by 14% and CVD mortality by 9%. At older ages (≥80 years), the corresponding relative risk is slightly lower, but the absolute risk is far greater than earlier in life17. For example, a 20 mm Hg difference in systolic BP between 120 and 140 mmHg is associated with an annual difference in absolute risk that is nearly ten times larger at ages 80-89 years than that at ages 50-59 years17.

MECHANISMS/PATHOPHYSIOLOGY

BP regulation

BP is determined by several parameters of the cardiovascular system, including blood volume and cardiac output (the amount of blood pumped by the heart per minute) as well as the balance of arterial tone that is affected by both intravascular volume and neurohumoral systems (discussed in the following sections). The maintenance of physiological BP levels involves a complex interplay of various elements of an integrated neurohumoral system that includes the renin-angiotensin-aldosterone system (RAAS), the role of natriuretic peptides and the endothelium, the sympathetic nervous system (SNS) and the immune system ( Figure 2 ). Malfunction or disruption of factors involved in BP control in any of these systems can directly or indirectly lead to increases in mean BP, BP variability or both, over time resulting in target organ damage (for example, left ventricular hypertrophy and CKD) and CVD outcomes22.

The pathophysiological mechanisms responsible for hypertension are complex and act on a genetic background. Primary hypertension involves multiple types of genes; some allelic variants of several genes are associated with an increased risk of developing primary hypertension and are linked in almost all cases to a positive family history ( Box 1) This genetic predisposition, along with a host of environmental factors, such as high Na⁺ intake, poor sleep quality or sleep apnoea, excess alcohol intake and high mental stress, contribute to the development of hypertension. Finally, the probability of developing hypertension increases with aging, owing to progressive stiffening of the arterial vasculature caused by, among other factors, slowly developing changes in vascular collagen and increases in atherosclerosis. Immunological factors can also play a major part, especially on the background of infectious or rheumatological diseases such as rheumatoid arthritis. The mosaic theory of hypertension describes its multifaceted pathophysiology28,29.

Box 1.

A large GWAS of 2.5 million genotyped single nucleotide polymorphisms (SNPs) in >69,000 individuals of European ancestry from 29 studies demonstrated that most SNPs related to BP regulation and CVD risk involved natriuretic peptides198. SNPs in genes that encode precursors for ANP and BNP had been previously identified199, and two other loci were identified in this study, containing genes involved in natriuretic peptide and NO signalling pathways; both these pathways regulate cyclic guanosine monophosphate, which promotes vasodilation. A 2016 study identified 66 BP-associated loci, which were enriched for cis-regulatory elements in vascular endothelial cells, consistent with a role in BP control through modulation of vascular tone. This information prompted development of a genetic risk score to predict target organ damage4.

Gene deletion studies in rodent models have evaluated cardiac ANP and BNP as paracrine regulators of vascular regeneration. Deletion of the genes encoding ANP and BNP exaggerates cardiac fibrosis and increase adverse left ventricular (LV) remodelling38, and natriuretic peptide receptor A (NPRA) deficiency leads to increased BP, severe fibrosis and LV dysfunction. Further, deletion of the gene encoding the endothelial guanylyl cyclase-A (GC-A) receptor, a cell surface receptor for natriuretic peptides, leads to diminished vascular regeneration and angiogenesis in response to critical hind limb ischemia, as well as cardiac fibrosis and diastolic dysfunction.

Further, clinical studies have observed an association between certain corin gene polymorphisms and risk of pre-eclampsia and hypertension, particularly among African-American but not Chinese populations200.

Sodium homeostasis regulation

Sodium (Na⁺) is a crucial regulator of blood volume: high serum Na⁺ concentration promotes fluid (water) retention, thereby increasing blood volume and BP. When dietary Na⁺ increases in normotensive individuals, compensatory haemodynamic changes occur to maintain constant BP. These changes include reduction in renal and peripheral vascular resistance and increased production of nitric oxide (a vasodilator) from the endothelium. However, if the effect of nitric oxide is impaired or absent, an increase in BP occurs. Endothelial dysfunction is a risk factor for the development of salt sensitivity and subsequent hypertension. Salt sensitivity is defined as a marked elevation in BP following a Na⁺ load of ≥5 g and is characterized by an elevation of systolic BP of at least 10 mmHg within a few hours of ingestion. Salt sensitive individuals have underlying endothelial dysfunction due to genetic or environmental influences. In response to a high salt load these individuals generally manifest overproduction of transforming growth factor β (TGF-β), which increases the risk of fibrosis, and oxidative stress, and have limited bioavailable nitric oxide. Chronic high salt ingestion can result in endothelial dysfunction, even in salt-resistant individuals30, and also affects the gut microbiota, with resultant changes that contribute to increased salt sensitivity and the development of hypertension31. High salt intake also appears to drive autoimmunity by inducing T helper 17 (T H17) cells31. High salt intake in mice has been shown to deplete Lactobacillus murinus in the gut microbiota. Treatment of mice with L. murinus prevented salt-induced exacerbation of salt-sensitive hypertension by modulating T H17 cells31. In line with these findings, a moderate high-salt challenge in a pilot study in humans reduced intestinal survival of Lactobacillus spp., increased the activity of T H17 cells and increased BP31. Thus, the gut microbiota appears to contribute to salt sensitivity of BP and the pathogenesis of hypertension.

Renin-Angiotensin-Aldosterone System

The RAAS has wide-ranging effects on BP regulation, mediating Na⁺ retention, pressure natriuresis (that is, the mechanism whereby increases in renal perfusion pressure (the gradient between renal arterial and venous blood pressure) lead to decreased Na⁺ reabsorption and increased Na⁺ excretion), salt sensitivity, vasoconstriction, endothelial dysfunction and vascular injury, and plays an important part in the pathogenesis of hypertension22. The RAAS is present at the cellular level in many organs, but its most crucial role is to help regulate pressure-volume homeostasis in the kidney, where it maintains perfusion in volume depleted states (that is, when there is a reduction in extracellular fluid volume as a result of sodium and fluid loss) and is suppressed in volume expanded (fluid overload) conditions. Renin and its precursor pro-renin are synthesized and stored in the juxtaglomerular cells of the kidney and are released in response to various stimuli ( Figure 3 ). The main function of renin is to cleave angiotensinogen to form angiotensin I. Angiotensin-converting enzyme (ACE) cleaves angiotensin I to form angiotensin II, which is at the center of the pathogenetic role of the RAAS in hypertension ( Figure 3 )32..

Angiotensin II enhances Na⁺ reabsorption in the proximal tubule by increasing the activity of the sodium-hydrogen exchanger (NHE3), sodium-bicarbonate exchanger and sodium-potassium ATPase, and by inducing aldosterone synthesis and release from the adrenal glomerulosa22. Angiotensin II is also associated with endothelial dysfunction and has pro-fibrotic and pro-inflammatory effects, mediated in large part by increased oxidative stress, resulting in renal, cardiac and vascular injury. Angiotensin II is tightly linked to target organ damage in hypertension via these mechanisms22..

Angiotensin-converting enzyme 2 (ACE2) has emerged as an important modulator in the pathophysiology of hypertension, CVD and renal disease, owing to its role in metabolizing angiotensin II into angiotensin-(1-7)33. Ang-(1-7) induces systemic and regional vasodilation, diuresis and natriuresis, and exerts antiproliferative and antigrowth effects on vascular smooth muscle cells, cardiac myocytes and fibroblasts as well as glomerular and proximal tubular cells33. Ang-(1-7) also has cardiorenal protective effects that are mediated by the proto-oncogene Mas receptor through signalling pathways that include mitogen-activated protein kinases (MAPK), PI3K-AKT, NADPH oxidase, TGF-β1, the EGF receptor, and NF-κB activity.

Aldosterone plays a crucial part in hypertension: by binding to the mineralocorticoid receptor, it induces non-genomic effects (that is, without directly modifying gene expression) that include activation of the amiloride-sensitive sodium channel, commonly known as the epithelial sodium channel (ENaC) and result in the stimulation of renal Na⁺ reabsorption in the cortical collecting duct36. Aldosterone also has many non-epithelial effects that contribute to endothelial dysfunction, vasoconstriction and hypertension36,37. These include vascular smooth muscle cell proliferation, vascular extracellular matrix deposition, vascular remodeling, fibrosis, and increased oxidative stress36,37.

Natriuretic Peptides

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) play an important part in salt sensitivity and hypertension. They have important natriuretic and vasodilator properties that allow maintenance of Na⁺ balance and BP during Na⁺ loading38,39. Upon administration of a Na⁺ load, atrial and ventricular stretch leads to release of ANP and BNP, respectively, which leads to systemic vasodilation and decreased plasma volume (owing to fluid shifts from the intravascular to the interstitial compartment) and results in BP lowering40. Natriuretic peptides increase glomerular filtration rate via an increase in efferent arteriolar tone in volume-expanded states and inhibit renal Na⁺ reabsorption through both direct and indirect effects. Direct effects include decreased activity of Na⁺-K⁺-ATPase and the sodium-glucose co-transporter in the proximal tubule and inhibition of the epithelial sodium channel in the distal nephron. Indirect effects include inhibition of renin and aldosterone release39.

Natriuretic peptide deficiency promotes hypertension. Corin is a serine protease that is largely expressed in the heart and converts the ANP and BNP precursors pro-ANP and pro-BNP to their active forms. Corin deficiency has been associated with volume overload, heart failure and salt-sensitive hypertension41. Natriuretic peptide deficiency also predisposes to insulin resistance and type 2 diabetes mellitus. Obesity is associated with natriuretic peptide deficiency, probably through upregulation of the natriuretic peptide scavenger receptor NPR-C in adipose tissue42. Natriuretic peptides have therapeutic potential for the metabolic syndrome; the metabolic syndrome is a cluster of conditions (including high BP, high fasting glucose levels, abdominal obesity, high triglycerides and microalbuminuria) that occur together, increasing the risk of CVD and diabetes mellitus42.

The Endothelium

The endothelium is a major regulator of vascular tone and major contributor to salt sensitivity through NO. Endothelial cells produce a host of vasoactive substances, of which NO is the most important in BP regulation43,44. NO is continuously released by endothelial cells in response to flow-induced shear stress, leading to vascular smooth muscle relaxation through activation of guanylate cyclase and generation of intracellular cyclic guanosine monophosphate45. Interruption of NO production via inhibition of constitutively expressed endothelial NO synthase (eNOS) causes BP elevation and development of hypertension in animals and humans46. Studies to evaluate NO activity in humans have demonstrated decreased whole-body production of NO in patients with hypertension compared with normotensive controls46,47.

Endothelial cells also secrete a variety of other vasoregulatory substances, including vasodilators such as prostacyclin and endothelium-derived hyperpolarizing factors, and vasoconstrictors such as endothelin 1 (ET-1), locally generated angiotensin II and the prostanoids thromboxane A2 and prostaglandin A2. ET-1 is a potent vasoconstrictor that activates ET-A receptors in vascular smooth muscle48. Other vasodilating substances, secreted by a variety of cells types, such as calcitonin gene related peptide, adrenomedullin and substance P act primarily through increases in NO release from endothelial cells49,50. The glucose-regulating gut hormone glucagon-like peptide-1 (GLP-1) also has vasodilating properties51. The balance between these factors, along with NO and ET-1, determines the final effect of the endothelium on vascular tone52,48,53,51. Circulating ET-1 levels are not consistently increased in hypertension, but there is a trend toward increased sensitivity to the vasoconstrictor and hypertensive effects of ET-1 in individuals with hypertension53. ET-A receptor antagonists attenuate or abolish hypertension in a variety of experimental models and are effective in lowering BP in humans48,53.

Endothelial dysfunction plays a seminal part in the pathogenesis of hypertension. Normotensive offspring of parents with hypertension often have impaired endothelium-dependent vasodilation, which implies a genetic component in the development of endothelial dysfunction47. Endothelial dysfunction in the setting of chronic hypertension is related to a combination of direct pressure-induced injury and increased oxidative stress. Several enzyme systems, including NADPH oxidase, xanthine oxidase and cyclooxygenase, as well as decreased activity of superoxide dismutase generate reactive oxygen species47,54. Excess superoxide anions bind to NO, decreasing NO bioavailability and generating the pro-inflammatory oxidant, peroxynitrite. Decreased NO bioavailability is the central factor that links oxidative stress to endothelial dysfunction and hypertension47. Salt-sensitive individuals may be very sensitive to the hemodynamic stress of increased blood volume, leading to overproduction of TGF-beta, oxidative stress, and limiting bioavailable NO30. Angiotensin II, along with other factors, including cyclic vascular stretch as a result of BP changes, endothelin-1 (ET-1), uric acid, systemic inflammation, norepinephrine, free fatty acids, and tobacco smoking, enhances NADPH oxidase activity and plays a central part in the generation of oxidative stress in hypertension52.

Sympathetic Nervous System

Baroreceptors, mechanoreceptors that sense pressure changes of the circulatory system, are housed in various locations in the arterial tree, a key place being the carotid sinus, a dilated area at the base of the internal carotid artery just superior to bifurcation of the common carotid artery. When this artery is stretched by elevated BP, nerve bundles projecting from the baroreceptors in the carotid sinus send messages to the brain to reduce sympathetic outflow of nerve impulses or nerve traffic and, thereby, BP. The SNS is generally more activated in persons with hypertension than in normotensive individuals.58,59 SNS activity is also greater in individual with obesity, in men than in women, in younger than in older persons, and in those with advanced kidney disease.60,61 Many patients with hypertension are in a state of autonomic imbalance with increased sympathetic and decreased parasympathetic activity59,62. SNS hyperactivity is relevant to both the generation and maintenance of hypertension. Studies in humans have also identified markers (such as increased catecholamine spillover and sural nerve activity assessed by microneurography) of sympathetic overactivity in normotensive individuals with a family history of hypertension63. Among patients with hypertension, increasing severity of hypertension is associated with increasing levels of sympathetic activity measured by microneurography64,65. Plasma catecholamine levels, microneurographic recordings and systemic catecholamine spillover (the amount of catecholamines released from sympathetic nerves innervating blood vessels that enter the bloodstream) studies have given evidence of increased sympathetic activity in patients with hypertension who are obese, in those with the metabolic syndrome, and in those whose hypertension is complicated by heart failure or kidney disease65.

The importance of the SNS in the pathogenesis of hypertension has been defined in a variety of experimental models. Models of obesity-related hypertension demonstrate that increased renal sympathetic nerve activity and its attendant increase in renal sodium reabsorption are key factors in the maintenance of sustained hypertension62. In another animal model, rats that received daily infusions of phenylephrine for 8 weeks developed hypertension during the infusions; their BP normalized under a low salt diet after discontinuation of phenylephrine, but once re-challenged with a high salt diet, the animals became hypertensive again30. The degree of BP elevation on the high salt diet was directly related to the degree of renal tubulo-interstitial fibrosis and decrease in glomerular filtration rate, suggesting that catecholamine-induced hypertension causes renal interstitial injury and a salt-sensitive phenotype that persists even after sympathetic overactivity is no longer present. In addition, enhanced SNS activity results in alpha-1 adrenergic receptor mediated endothelial dysfunction, vasoconstriction, vascular smooth muscle proliferation and increased arterial stiffness, which contribute to the development and maintenance of hypertension66. Finally, there is evidence that sympathetic overactivity enhances salt-sensitivity owing to a reduction in activity of the WNK lysine deficient protein kinase 4 ( WNK4) gene, which encodes a serine/threonine kinase that inhibits the thiazide-sensitive-Na-Cl co-transporter, resulting in increased distal tubular Na⁺ retention67. These mechanisms have been reviewed recently66.

Inflammation and the immune system

Inflammation makes an important contribution to the genesis of hypertension and related target organ damage. Inflammation is associated with increased vascular permeability and release of potent mediators, such as reactive oxygen species, NO, cytokines and metalloproteinases. Cytokines mediate the formation of neo-intima (a new or thickened layer of arterial intima), thereby decreasing the lumen diameter of resistance vessels (small arteries and arterioles highly innervated by autonomic nerves and the primary vessels involved in the regulation of BP), and promoting vascular fibrosis, leading to increased vascular resistance and stiffness. Cytokines also affect renal tubular function by increasing local synthesis of angiotensinogen and angiotensin II, as well as promoting sodium and volume retention in hypertension68. Matrix metalloproteinases stimulate the degradation of the extracellular matrix, allowing infiltration of immune cells through the vessel wall into the interstitium of the affected organs, promoting apoptosis and enhancing collagen synthesis and matrix deposition, leading to target organ damage68.

While animal data are clear about the relationship between inflammation and hypertension, the data in humans are limited. There are associations between C-reactive protein, TNF-alpha and various interleukins and hypertension, but no direct link68. GWASs have identified a single nucleotide polymorphism of SH2B3 (SNP rs3184504), which results in an amino acid substitution in SH2B adapter protein 3 (a protein involved in T cell receptor activation and signalling), that is associated with many autoimmune and cardiovascular disorders, including hypertension69. Further, drugs that are used to treat inflammation, such as non-steroidal anti-inflammatory drugs and cyclosporine, raise rather than lower BP in hypertensive individuals, highlighting the complex nature of the relationship between inflammation and hypertension69.

Both innate and adaptive immune responses participate in the generation of reactive oxygen species and inflammatory changes in the kidneys, blood vessels and brain in hypertension68,70. Innate immune responses, especially those mediated by macrophages, have been linked to hypertension induced by angiotensin II, aldosterone and NO antagonism68,70. Reductions in macrophage infiltration of the kidney or the peri-adventitial space of the aorta and medium sized arteries lead to reductions in BP and salt-sensitivity68. Adaptive immune responses via T cells have also been linked to the genesis of hypertension and its target organ damage. T cells express AT1 receptors and mediate angiotensin II-dependent hypertension,70 and it has been shown that depletion of mature lymphocytes ameliorated hypertension and kidney injury resulting from a high-salt diet in the Dahl SS rat71. Thus, a balance between proinflammatory T cell reactivity and inflammatory suppression induced by T regulatory cells determines the development of hypertension, as demonstrated by the amelioration of hypertension with the adoptive transfer of T regulatory cells in several animal models of hypertension68-70. Abnormalities in both pro-inflammatory T cells and regulatory T cells are implicated in hypertension-induced target organ damage, as they regulate the inflammatory processes in the kidney and vasculature that underlie hypertension-induced kidney disease

DIAGNOSIS, SCREENING AND PREVENTION

Diagnosis and screening

Essential or primary hypertension is usually asymptomatic; thus, in clinical practice all adults should have their BP measured at regular office visits. Hypertension is most commonly diagnosed based on repeated BP measurements in a clinical office setting. Accurate measurement and recording of BP is essential to categorize the level of BP, ascertain BP-related CVD risk and guide management. Since 2010, methods to measure out-of-office BP have been increasingly introduced to guide diagnosis and treatment of hypertension72,73. Table 1 These include home BP monitoring (HBPM) and ambulatory BP monitoring (ABPM). HBPM refers to the measurement of BP at regular intervals by an individual at their home or elsewhere outside the clinic setting. ABPM consists of measuring and recording the BP at regular intervals (usually every 20-30 minutes), typically for the 24-hour period and while individuals go about their daily activities. The ability to measure out-of-office BP has enabled the identification of distinct BP phenotypes, including white coat or isolated clinic hypertension and masked or isolated ambulatory hypertension74,75. White coat hypertension is characterised by elevated office BP but normal ABPM or HBPM readings. By contrast, masked hypertension is characterised by normal office readings but elevated out -of-office readings ( ABPM and HBPM )74,75.

Diagnosis

The evaluation of a patient with hypertension requires more than the diagnosis of elevated BP. It should also include assessment of the CVD risk, target organ damage, and concomitant clinical conditions that may affect the BP or related target organ damage as well as recognition of features suggestive of secondary hypertension. Some of these investigations are routine tests necessary in all patients, but others only in specific patient groups identified by history, clinical examination, and routine tests. In rare inherited forms of hypertension, a single gene mutation explains the pathogenesis of hypertension7,8,9. ( Figure 4 ) A small proportion of patients have a potentially reversible cause of hypertension, and a correct diagnosis might lead to a cure or a substantial improvement in BP control with a reduction of CVD risk. It is therefore appropriate to implement a simple screening for secondary hypertension in all patients. The screening is based on clinical history, physical examination and routine laboratory investigations ( Box 2 and 3). Secondary hypertension should also be considered in cases of a sudden worsening of hypertension, poor BP response to drug treatment or severe target organ damage, which is out of proportion to the duration and severity of hypertension. In these cases, specific diagnostic tests are indicated ( Table 2 ).

Table 2 -

Possible causes

Clinical indications

Diagnostics

Clinical history

Physical examination

Laboratory investigations

First-line test(s)

Additional confirmatory test(s)

Common causes

Renal parenchymal disease

● History of urinary tract infection or obstruction, haematuria (blood in the urine), analgesic abuse
● family history of polycystic kidney disease

Abdominal masses (in case of polycystic kidney disease)

● Presence of protein, erythrocytes, or leucocytes in the urine
● decreased GFR

Renal ultrasound

Detailed work-up for kidney disease

Renal artery stenosis

● Fibromuscular dysplasia: early onset hypertension (especially in women).
● Atherosclerotic stenosis: hypertension of abrupt onset, worsening or increasingly difficult to treat; flash pulmonary oedema

Abdominal bruit (abnormal sound)

● Difference of >1.5 cm in length between the two kidneys (renal ultrasound),
● rapid deterioration in renal function (spontaneous or in response to RAA blockers)

Renal Duplex Doppler ultrasonography

● Magnetic resonance angiography,
● spiral computed tomography
● intra-arterial digital subtraction angiography

Primary aldosteronism

● Muscle weakness
● family history of early onset hypertension and cerebrovascular events at <40 years of age

Arrhythmias (in case of severe hypokalaemia)

● Hypokalaemia (spontaneous or diuretic-induced)
● incidental discovery of adrenal masses

Aldosterone-renin ratio under standardized conditions (corrected hypokalaemia and withdrawal of drugs affecting RAA system)

● Confirmatory tests (oral sodium loading, saline infusion, fludrocortisone suppression, or captopril test)
● adrenal CT scan
● adrenal vein sampling

Uncommon causes

Pheochromocytoma

● Paroxysmal hypertension or a crisis superimposed to sustained hypertension;
● headache, sweating, palpitations and pallor;
● positive family history of pheochromocytoma

Skin stigmata of neurofibromatosis (café-au-lait spots, neurofibromas)

Incidental discovery of adrenal (or in some cases, extra-adrenal) masses

Measurement of urinary fractionated metanephrines or plasma-free metanephrines

● CT or MRI of the abdomen and pelvis;
● ¹²³I-labelled meta-iodobenzyl-guanidine scanning;
● genetic screening for pathogenic mutations

Cushing syndrome

● Rapid weight gain,
● polyuria (excessive production of urine),
● polydipsia (excessive thirst),
● psychological disturbances

Typical body habitus (central obesity, moon-face, buffalo hump, red striae (stretch marks), hirsutism)

Hyperglycaemia

24-h urinary cortisol excretion

Dexamethasone-suppression test

Box 2 -

Box 3 -

The medical history has to address the time of the first diagnosis of hypertension, current and past BP measurements and antihypertensive medications. A history of pregnancy-related hypertension is an important factor in the assessment of women with hypertension. Hypertension results in an increased risk of CVD complications, and chronic kidney disease (CKD). Thus, a careful medical history should be taken in all patients to allow for assessment of global CVD risk, with special emphasis on current and past smoking habits and evidence of dyslipidaemia and diabetes mellitus. CVD risk should be estimated using an established calculator (e.g. http://ASCVD-Risk-Estimator/). Adults at high risk for CVD have a high probability to benefit from antihypertensive drug therapy in addition to lifestyle change76.

The physical examination aims to establish the diagnosis of hypertension and screen for target organ damage and secondary causes ( box 2). The patient should sit quietly for 5 minutes before a BP reading is taken and BP cuff should be at heart level. An average of 2 to 3 BP measurements obtained at 2 to 3 separate occasions provides an accurate basis for estimation of BP77,78. At least once, BP should be measured on both arms, and differences in SBP > 20 mmHg and/or in DBP >10mmHg should initiate investigations of vascular abnormalities77. Careful attention should be paid to choosing appropriately sized cuff, particularly for the increasing number of patients with obesity. Further, BP should be measured in both sitting and standing positions to rule out orthostatic hypotension (a sudden drop of the BP when a person stands up from a lying or sitting position). This is particularly important in elderly individuals.

All patients should undergo auscultation of the carotid arteries, heart and renal arteries. Detection of murmurs (sounds audible via the stethoscope) should lead to further investigations: carotid ultrasound, echocardiography and renal ultrasound, respectively. An irregular pulse frequently indicates atrial fibrillation, which should be confirmed by an electrocardiogram (EKG). Laboratory investigations are used to detect additional risk factors, to confirm or exclude secondary hypertension, to detect clinical or subclinical target organ damage and to estimate global CVD risk ( box 3).

Prevention

The association between BP and risk of CVD highlights the importance of treating hypertension, especially when severe. Further, it also underscores the importance of strategies to reduce BP-related CVD risk in those who have a higher than normal level of BP (average systolic BP 120-129 mmHg) but below the hypertension threshold. Reducing BP in adults with a high normal BP (referred to as elevated BP in the 2017 US guidelines) provides the potential to directly reduce CVD risk and to prevent or at least slow the age-related tendency for individuals to develop hypertension.

In most countries there is a strong tendency for BP, especially systolic BP, and the prevalence of hypertension to increase progressively from childhood until late in life79. However, studies in isolated societies that have limited contact with the outside world84,85 indicate that high BP is not an inevitable consequence of aging and that the rise in BP associated with local migration by members of isolated societies is related to changes in diet, decreased physical activity and consumption of alcohol. These reports underscore the logic of efforts to prevent high BP in settings where an age-related increase in BP is common.

Lifestyle changes

A variety of nonpharmacological interventions have been shown to be effective in lowering BP and preventing hypertension. The most effective interventions are weight loss88,89,90, reduced Na⁺ intake88,89,90,91, increased potassium intake92,93, increased physical activity94, reduced consumption of alcohol95,96 and diets like the Dietary Approaches to Stop Hypertension (DASH) diet97 that combine several elements which favorably affect BP98,99 ( table 3 ). The DASH diet is especially successful when combined with other effective BP lowering interventions such as a reduced intake of dietary sodium91. Lifestyle change is the best way for the individual to implement these interventions. Even small improvements in an individual's lifestyle can be valuable. Government agency and professional society websites provide helpful tips for lifestyle change and monitoring of BP. Careful monitoring of BP is essential because the beneficial effects of lifestyle change are predicated on maintenance of the intervention100.

Table 3.

Food group

Servings*

Examples of a serving

Whole grains

6-8 per day

1 slice whole grain bread

Vegetables

4-5 per day

1 cup of raw leafy vegetables

Fruits

4-5 per day

1 medium sized fruit

Dairy products (low-fat or fat-free)

2-3 per day

1 cup of milk or yogurt

Fats and oils

2-3 per day

1 teaspoon of margarine or vegetable oil or
1 tablespoon of mayonnaise or
2 tablespoons of salad dressing

Lean meat, poultry, fish

2-3 per day

2 ounces of cooked meats, chicken or fish

Nuts, seeds and legumes

4-5 per week

1/3 cup (1.5 ounces) of nuts or
2 tablespoons of peanut butter or
2 tablespoons (0.5 ounce) of seeds or
½ cup of cooked peas or beans

Candy and added sugars

5 or less per week

1 tablespoon of sugar, jelly or jam or
1 cup of lemonade

Two complementary strategies aimed at achieving a small population-wide reduction in BP or a larger reduction in those who are at higher risk to develop hypertension can be employed to implement hypertension prevention interventions98,99,101. Modeling studies suggest that a downward shift of as little as 2 mmHg in the population distribution of diastolic BP would result in a 17% reduction in the incidence of hypertension, a 14% reduction in the risk of stroke and transient ischemic attacks, and a 6% reduction in the risk of coronary heart disease102. Public health interventions focused on dietary improvements and increases in physical activity that are known to lower BP provide the basis for the population-wide strategy. Diet in the general population can be favorably influenced by means of public health education campaigns, food product labeling, and collaborations with food manufacturers to reduce the calorie and sodium content of their products, as well as with fast food companies and restaurants to reduce portion size and to promote healthier food preparation and promotion practices. Physical activity can be enhanced by making it easier for members of the community to engage in exercise on a routine basis.

Pharmacological interventions

Low-dose pharmacological therapy has also been shown to be effective in lowering BP and preventing hypertension in three randomized controlled trials conducted in adults with high normal BP103,104,105. The Brazilian multi-center PREVER-Prevention Trial compared treatment with the low-dose long-acting thiazide-like diuretic chlorthalidone in combination with the potassium sparing agent amiloride with treatment with placebo105. Treatment with the low-dose chlorthalidone and amiloride combination resulted in both a decrement in BP and prevention of hypertension and a reduction in left ventricular mass. A drug intervention is easier to implement and maintain than a lifestyle change intervention but there is a natural reluctance to recommend a lifetime of pharmaceutical therapy for prevention of hypertension. Consideration of low-dose pharmacotherapy should be restricted to those who are at high risk of developing hypertension despite energetic efforts to lower BP by means of one or more nonpharmacological interventions105.

MANAGEMENT

BP treatment thresholds and targets

Until 2015, most guidelines recommended a target BP < 140/90 mmHg for most patients and < 150/90 mmHg for elderly patients over 60 or 80 years of age ( Table 4 )77,106. However, after the publication of the Systolic blood PRessure Intervention Trial (SPRINT)107, target systolic BP values have been frequently debated. SPRINT was a randomized, open-label controlled trial that enrolled 9361 participants without diabetes mellitus but with increased CVD risk. Patients with a history of stroke were excluded. Participants were randomized to a standard systolic BP target < 140 mmHg or intensive systolic BP target < 120 mmHg. Intensive BP treatment in SPRINT resulted in a significantly greater (25%) reduction in the primary endpoint (first occurrence of myocardial infarction, acute coronary syndrome, stroke, heart failure or death from cardiovascular causes), compared with standard treatment. Office BP measurement in SPRINT was performed with an automated device timed to start measurement after 5 minutes of rest in an effort to standardize measurements in the various clinics and minimize the white coat effect. Because large differences had been observed between automated office BP measurement and conventional auscultatory measurements (with the automated technique showing lower values)108, some groups have questioned the applicability of the SPRINT intensive systolic BP target of < 120 mmHg to ordinary office practice109. Both the appropriate method(s) of measuring office BP (automated versus manual; unattended versus attended) and the appropriate BP targets for antihypertensive treatment are currently topics of vigorous debate. In summary, newer guidelines published after the SPRINT trial generally have more aggressive goals, at least for individuals < 65 years of age ( Table 4 ).

Table 4.

Guideline

Population

Goal BP (mmHg)

Adults 65 years and older

<150/90 (<140/90 if tolerated)

Adults with diabetes, CHD or renal disease

<130/80

Adults > 80 years

< 150/90

Adults with diabetes

< 140/85

Adults with CKD without proteinuria

< 140/90

Adults with CKD with overt proteinuria

< 130/90

Adults with CHD

< 140/90

Young adults

< 130/80

Elderly > 80 years

< 150/90

Adults ≥ 60 years

< 150/90

Adults with diabetes

< 140/90

Adults with CKD

< 140/90

Adults > 80 years

SBP 140-150

Late phase elderly patients

<150/90 (<140/90 if tolerated)

Adults with diabetes or CKD

< 130/80

Adults with CHD or CVD

< 140/90

Adults ≥ 80 years

< 150

High-risk adults ≥ 50 years

≤ 120*

Adults with diabetes in whom prevention of stroke is priority

< 120

Adults with diabetes and high risk for CVD

< 130/80

Adults without additional markers of increased CVD risk

< 130/80

Older adults ≥ 65 years of age,
noninstitutionalized, ambulatory

< 130/80

Older adults ≥ 65 years of age, with comorbidities and limited life expectancy

Individualized goal based on clinical judgement and patient preference

Patient's global CVD risk and comorbidities should be considered in determining the need for pharmacologic antihypertensive treatment. The 2017 US ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation and Management of High Blood Pressure in Adults110 recommend the use of antihypertensive medication in patients with pre-existing CVD and those without a CVD event but an estimated 10-year atherosclerotic cardiovascular disease (ASCVD) risk of 10% or higher at BP levels ≥ 130/80 mmHg. In individuals without CVD and with 10-year ASCVD risk < 10%, antihypertensive medication should be initiated at BP ≥ 140/90 mmHg. ( Figure 5 ).

Non-Pharmacological Management

Lifestyle advice is recommended for all patients with hypertension. The most effective interventions are the same as for prevention of hypertension. Targeted dietary approaches can reduce the systolic BP in individuals with hypertension. For example, reducing sodium intake (ideally to <2.3 g per day, or <1.5 g per day in those most susceptible to the effects of sodium on BP, but reduction by at least 1.0 g per day is desirable) can lower the systolic BP by 2-4 mmHg (Ref). A similar reduction can be expected with increases in potassium intake to 3.5- 5.0 g per day92.

Reduced salt intake

For metabolic balance, the amount of salt consumed must be equal to that lost. Thus, under normal living conditions and physical activity levels, an intake of 5 g salt/day is considered sufficient, in line with the WHO recommendation (< 5 g per day)113. By contrast, the currently estimated dietary intake of salt is about 9-12 g per day in most countries. The current recommendations of the American Heart Association114 and American Society of Hypertension115 are stricter than the European guidelines, recommending lowering salt intake to 3.8 g per day, whereas the 2013 ESH/ESC guidelines recommend 5-6 g of salt per day77.

There is strong evidence to support population-wide recommendations to lower salt intake119,120. As more than 75% of dietary salt comes from processed foods (in western countries), any population strategy to reduce salt intake must involve food manufacturers and restaurants, in order to progressively reduce salt added to foods. So far, only three countries (Japan, Finland and the United Kingdom) have successfully reduced population salt intake121.

Moderate alcohol consumption

Keeping alcohol intake ≤2 standard drinks (~3.5 alcohol units) per day for men and ≤1 standard drink (~1.75 alcohol units) per day for women can also contribute to a 2-4 mmHg BP reduction. 95,96

Physical activity

Regular physical activity reduces BP in individuals with hypertension. Endurance training reduces BP more in persons with hypertension than in individuals with normal BP. A narrative review of 27 randomized clinical trials in individuals with hypertension showed that regular medium-intensity to high-intensity aerobic activity reduced BP by a mean of 11/5 mmHg125. Sessions lasting 40-60 minutes performed at least three times a week had the greatest effect on BP. Three randomized controlled trials of isometric exercise (strength training) showed a BP reduction of similar magnitude to that induced by aerobic exercise in individuals with hypertension125. A meta-analysis of 64 controlled studies of the efficacy of dynamic resistance training as stand-alone antihypertensive therapy showed BP reductions comparable with or greater than those with aerobic exercise training126. Greater BP reductions occurred in individuals with higher resting BP (approx. 6/5 mmHg for individuals with hypertension and 3/3 mmHg for individuals with pre-hypertension) and in non-white individuals126.

Weight Loss

Excess adiposity generally raises BP in susceptible individuals, and patients with hypertension who also have obesity require more antihypertensive medications to control their BP and are more likely to be treatment resistant127. In a recent meta-analysis, any reduction in body weight lowered systolic BP by on average 2.69 mmHg and in diastolic BP by on average 1.34 mmHg (Ref128). However, the response varies substantially between individuals. Lifestyle interventions, including hypocaloric diets and physical exercise, are commonly recommended for patients with obesity and hypertension, yet average weight loss is modest and most patients regain weight129 ( box 4).

Box 4

Weight loss is recommended for individuals with obesity, and may be particularly important if these patients also have hypertension. Medications have been developed for the treatment of obesity, but their approval status differs between the United States and Europe: some drugs are only approved in the United States (for example, lorcaserin and topiramate/phentermine), whereas others are approved in Europe only. BP reductions in patients with hypertension have been reported for some weight loss medications201, but their specific pharmacological actions may attenuate the positive influences of weight loss on BP and CVD outcomes133. Bariatric surgery is very effective in reducing body weight, and the risk for arterial hypertension is substantially reduced up to five years following bariatric surgery202. However, large and sustained body weight reductions are needed to substantially reduce BP following bariatric surgery203 and there are no large clinical trials specifically testing the effects of weight loss medications or bariatric surgery on hypertension control.

Antihypertensive Pharmacotherapy

Antihypertensive pharmacotherapy has evolved over several decades driven by development of various antihypertensive medication classes and large-scale outcomes trials proving their benefits on CVD morbidity and mortality130. Clinicians are now faced with a plethora of antihypertensive medications of different drug classes and a variety of fixed dose combinations. Typically, antihypertensive pharmacotherapy begins with first-line antihypertensive medications either in monotherapy or in combination131. Combination therapy may be preferable in patients with higher levels of pretreatment BP. First-line antihypertensive medications include ACE inhibitors, angiotensin II receptor blockers (also known as sartans), dihydropyridine calcium channel blockers, and thiazide diuretics106. Beta-blockers are also indicated in patients with heart failure and reduced left ventricular ejection fraction or post myocardial infarction, and some guidelines recommend beta-blockers as first line antihypertensive medications 77,132. The choice should be based on individual efficacy and tolerability. Ethnicity affects the response to antihypertensive medications, and it has been suggested that calcium channel blockers and diuretics may be the first choice in blacks. Further, in specific clinical situations, for example hypertension in pregnant women, other medications such as alpha-methyldopa (an agonist of alpha adrenoreceptors in the central nervous system that inhibits the sympathetic nervous system) or labetalol (a beta adrenoreceptor blocker) are preferable, whereas some first line antihypertensives, for example ACE inhibitors and angiotensin II receptor blockers, are contraindicated because of increased risk for renal teratogenicity. Divided dosing of antihypertensive drugs tends to decrease adherence and should be avoided when possible135.

BP cannot be controlled with monotherapy in many patients, particularly those with severe hypertension. When combining antihypertensive medications, it is important to consider whether the drugs have additive effects on BP or adverse effects, and whether the patient has comorbidities that mandate particular drug choices77. ACE inhibitors or angiotensin II receptor blockers, thiazide diuretics and dihydropyridine calcium channel blockers are additive in lowering BP and can be combined as double or triple combination therapies. By contrast, combining ACE inhibitors and angiotensin II receptor blockers adds little BP lowering while increasing the risk for renal dysfunction and hyperkalemia (high blood potassium levels, which can lead to cardiac arrhythmias). Similarly, combining RAAS inhibitors with beta-adrenoreceptor blockers adds little BP reduction, but this combination is indicated in patients following acute myocardial infarction or heart failure with reduced left ventricular ejection fraction for reasons beyond BP reduction.

Dihydropyridine calcium channel blockers.

Dihydropyridine calcium channel blockers elicit vasodilation by blocking vascular smooth muscle L-type calcium channels. They are effective antihypertensive drugs with extensive experience in large clinical trials136. A practical advantage of this drug class is that it can be combined with all other first-line antihypertensives. Peripheral edema, which is explained by peripheral arterial vasodilation rather than worsening heart failure or kidney dysfunction, is a common side effect, particularly in individuals with obesity. Non-dihydropyridine calcium channel blockers, especially verapamil, also inhibit cardiac calcium channels, which can reduce heart rate and cardiac contractility141. Calcium channel blockers can induce or worsen constipation, especially in institutionalized older persons142. All calcium channel blockers modestly inhibit the drug metabolizing enzyme cytochrome P450 3A4, and, therefore, could elicit important drug-interactions143.

Thiazide-type and thiazide-like diuretics.

Thiazide-type diuretics (for example, hydrochlorothiazide) have a benzothiadiazine ring, whereas thiazide-like diuretics (for example, chlorthalidone, metolazone and indapamide) lack the benzothiadiazine structure. Both subclasses of thiazide diuretics inhibit Na⁺ and CI⁻ co-transporters in renal tubules, thereby promoting natriuresis, and have been an important component of pharmacological hypertension management ever since the first trials showing morbidity benefits of antihypertensive therapy144. Over the years, diuretic doses have been substantially reduced to attain better risk-benefit profiles. Thiazide-type and thiazide-like diuretics can worsen glucose metabolism increasing the risk for new onset diabetes mellitus, but whether or not this metabolic action translates into long-term increases in CVD risk has been called into question145. Hydrochlorothiazide, the most commonly prescribed thiazide-type diuretic worldwide, may be less effective in mitigating CVD risk compared to chlorthalidone or indapamide146,147. Drug-related electrolyte disturbances, including hypokalemia and hyponatremia (low blood potassium and sodium levels, respectively), are particularly important adverse effects; hypokalemia can lead to cardiac arrhythmias and muscle weakness, and hyponatremia can cause confusion, seizures and coma. The risk for hypokalemia is reduced when thiazide-type and thiazide-like diuretics are combined with potassium supplements or potassium-sparing agents, such as ACE inhibitors, angiotensin receptor blockers, or potassium-sparing diuretics. Hyponatremia is a potentially life threatening adverse effect, particularly in elderly persons.

Beta-adrenoreceptor blockers.

Beta-adrenoreceptor blockers lower BP reducing cardiac output, heart rate, renin release and adrenergic control nervous system effects148. They improve outcomes following acute myocardial infarction and in patients with heart failure with reduced left ventricular ejection fraction, but, in the absence of these comorbidities, beta-adrenoreceptor blockers are inferior to other first line antihypertensives in reducing CVD morbidity and mortality149. This effect has been attributed to lesser reductions in aortic BP150 and adverse effects on body weight151 and glucose metabolism with beta-adrenoreceptor blockade. Some of these disadvantages might be mitigated with newer vasodilator beta-adrenoreceptor blockers, such as nebivolol and carvedilol152. However, there are no large-scale antihypertensive trials demonstrating that this difference translates into better clinical outcomes. Beta-adrenoreceptor blockers may promote bronchial obstruction is patients with asthma and should not be combined with non-dihydropyridine calcium channel blockers such as verapamil that lower sinus node rate or atrioventricular conduction.

Treatment Resistant Hypertension

Treatment resistant hypertension is commonly diagnosed when office BP is >140/90 mmHg despite treatment with three or more properly dosed antihypertensive drugs including a diuretic and secondary hypertension has been ruled out159. Poor treatment adherence is a common cause of apparent treatment resistant hypertension. The true prevalence of treatment resistant hypertension is unknown, but an estimated 12.8% of all individuals with hypertension in the United States and 15.3 % of those treated with antihypertensives fulfill the criteria for treatment resistant hypertension160. Adding a fourth or fifth drug could lead to satisfactory BP control in these patients. The PATHWAY trial rotated patients with treatment resistant hypertension through different add on drugs or placebo in a randomized fashion161. All patients received a standardized antihypertensive regimen comprising three drugs, including a diuretic. Compared with alpha-adrenoreceptor or beta-adrenoreceptor blockade, the mineralocorticoid receptor antagonist spironolactone was the most effective fourth antihypertensive drug. In another study in patients whose BP was uncontrolled despite receiving three drugs, sequential addition of a mineralocorticoid receptor antagonist followed by a loop diuretic (which acts at the ascending limb of the loop of Henle in the kidney) was more effective than adding an ACE inhibitor followed by a beta-adrenoreceptor blocker162. Overall, mineralocorticoid receptor antagonism is a reasonable choice in patients with difficult to control hypertension. Given the risk of inducing hyperkalemia163, serum potassium concentrations should be monitored.

Device-based Treatments

Device-based treatments have been primarily developed for patients with severe resistant hypertension whose BP cannot be controlled with antihypertensive drugs156. Catheter-based renal nerve ablation164,165, electrical carotid sinus stimulation166,167, modulation of baroreflex transduction with a dedicated carotid stent168, carotid body denervation169, and deep brain stimulation170 are thought to lower BP through SNS inhibition. Creation of a defined arteriovenous stent with a coupler device lowers BP by reducing peripheral vascular resistance171. These treatments are in various stages of clinical development, with the most extensive data available on renal nerve ablation and electrical carotid sinus stimulation. None has yet been proven efficacious in lowering BP in randomized sham-controlled clinical trials164,161,167, because either the primary endpoint was not achieved or no trials have been conducted. Finally, trials with hard clinical endpoints do not exist.

QUALITY OF LIFE

Health-related quality of life (HRQoL) is a multi-dimensional concept that includes domains related to physical, mental, emotional, and social functioning; studies demonstrate that each additional disease, as well as the severity of these diseases, is associated with declines in HRQOL 172. Population-based studies have consistently shown that being diagnosed with hypertension is associated with worsening of HRQoL even after adjusting for other comorbidities173,174. Altered HRQoL in persons with hypertension has been attributed to a variety of factors, including the diagnosis, treatment, and effects of alterations (both elevations and reductions) in BP173.

Antihypertensive medication use is associated with a variety of symptoms that could lower HRQoL177. Observational studies showed an association between the number of antihypertensive medications prescribed and worsening of the HRQoL178. Some classes of antihypertensive medications, (for example, ACE inhibitors) are better tolerated than others (for example, beta blockers and centrally acting agents, such as alpha-methyldopa) and result in significantly better scores on measures of general well-being179. Further, small differences in HRQoL have even been reported among medications of the same class, e.g., enalapril vs. captopril180. However, clinical trials with newer antihypertensive agents have generally indicated that they are extremely well-tolerated and can enhance the effects of non-pharmacological treatment on HRQoL177,181. In the Treatment of Mild Hypertension Study (TOMHS), combining lifestyle modifications with any of five different antihypertensive medication classes resulted in greater improvements in HRQoL than lifestyle modifications plus placebo181.

Treatment-related reductions in BP could have a negative effect on HRQoL, particularly in older and more frail patients at high risk of hypotension. Clinical trials performed in the 1990s that evaluated patients with very high baseline BP, for example, the Systolic Hypertension in the Elderly Program Trial (SHEP) and the Systolic Hypertension in Europe Trial (Syst-Eur), generally found minimal effects of BP reductions on HRQoL182,183. Two more recent clinical trials have targeted lower BPs (intensive systolic BP target < 120 mmHg versus standard systolic BP target < 140 mmHg ), it had been postulated that this lower BP might be expected to cause cerebral hypoperfusion, resulting in falls, dizziness, and cognitive impairment184,185,107. In a substudy of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) study, HRQoL was evaluated in 1,028 participants randomized to either intensive or standard therapy. No differences in mental function were noted between treatment groups, but intensive therapy was associated with a small, not clinically significant, decrease in physical function185. In the Systolic Blood Pressure Intervention Trial (SPRINT), targeting systolic BP <120 mmHg required 1 additional antihypertensive medication compared to standard treatment to target systolic BP < 140 mmHg and was generally safe and well tolerated107,186. Compared to standard treatment, intensive treatment did not affect the perceived HRQOL of SPRINT participants, measured by patient reported outcomes of physical and mental health, self-reported satisfaction with care and medication adherence, even when stratifying on age and comorbidities186. Almost 90% of participants in both treatment groups reported satisfaction with their BP care, and more than 1/3 described improvement in satisfaction over baseline levels.

Quality of life concerns remain an important aspect of hypertension management. SPRINT has demonstrated that with careful clinical management, lower BP can be targeted without concern of worsening physical and mental function. Clinicians must seek the optimal balance of reducing CVD morbidity and mortality while maximizing well-being for each individual patient.

OUTLOOK

Overall, prevention will probably contribute least to any improvement in BP-associated disease burden. This is because 80% of the world is in the process of developing, which hitherto has inevitably been associated with increased exposure to the main environmental determinants of raised BP such as excess intake of calories, alcohol and salt. Food and drink industries, governments and education systems would be required to cooperate in order to reverse this pattern

Implementation of preventive strategies has largely been limited to high income countries. Despite reasonably compelling evidence to the contrary111, recommendations that the general population should restrict salt intake have been questioned on the basis of largely suboptimal observational data189. Such confusion worsens an already very difficult public health challenge. Data show that only approximately half of people with hypertension are aware of their condition190, and the Lancet Commission on hypertension identified improving awareness of hypertension is a critical action needed to improve the current disease burden191,192. The global BP awareness campaign promoted by the International Society of Hypertension whereby World Hypertension Day was extended to become May Measurement Month (MMM) in 2017 could contribute substantially to improving rates of routine BP screening around the world83. Over 1.20 million adults (≥18 years) from >100 countries were screened as part of MMM and the ensuing data allied to health-economic analyses will be used to persuade policy makers in each country that enhanced local BP screening and treatment facilities are wise financial investments.

Meanwhile, single-pill formulations of the drug combinations most commonly recommended in current guidelines (calcium channel blocker plus a diuretic, calcium channel blocker plus a RAAS-blocker or diuretic plus a RAAS-blocker) are readily available and have low production costs. In addition, a 3-drug combination of a calcium channel blocker, a diuretic and a RAAS-blocker132 should also be produced for more severe hypertension, with low dose spironolactone available as a fourth-line agent161. Hence, 1 or 2 tablets will be able to control BPs of all but a small proportion of patients with hypertension.

These formulations should be made available and affordable in all countries of the world.191 Additional local obstacles to the distribution and delivery of these agents to patients with hypertension within each country will also have to be overcome - among which the lack of effective screening programmes is crucial191.

Antihypertensive medications are prescribed by different health professionals in different countries. However, even in high income countries, much of the "routine" uncomplicated hypertension management could, and probably should be carried out by nurse practitioners or other non-physician health workers. In more remote parts of the world, the use of e-healthcare techniques196 should be increasingly used to facilitate task-shifting or task sharing by non-physician health-workers where doctors are unavailable197.

In summary, although there are many interesting unanswered scientific research questions in the field of hypertension ( Box 5), perhaps the most pressing need to reduce the diseas burden is to evaluate the best way(s), at a local level, to screen routinely for raised BP and then to deliver the best, most affordable, evidence-based combination of antihypertensive agents. Meanwhile, efforts to drive public health policy towards encouraging more healthy diets and lifestyles from a BP and CVD viewpoint should be encouraged and basic scientific research that might allow precision medicine to be applied to patients with hypertension must also continue.

Box 5

Measurement Issues

Is hypertension management improved by basing treatment strategies on serial unattended office BP measurements, out of office (home or ambulatory) BP measurements or central BP measurements?

How should BP be measured in patients with atrial fibrillation?

Treatment Issues

Should salt restriction at the population level continue to be recommended at current targets?

To what extent should age, estimated CVD risk and concomitant conditions influence treatment thresholds?

Should white-coat hypertension be treated?

If management strategy is to be influenced by central or out of office BP levels, what treatment thresholds and targets should be used?

Should reducing 24-hour and longer-term BP variability be a consideration in the selection of drug treatment for optimal CVD protection?

What combinations of antihypertensive agents give optimal CVD protection, stratified by age and ethnicity?

What is the optimal BP treatment target stratified by age, CVD risk and concomitant disease status?

What is the optimal management of treatment resistant hypertension that is resistant to 4 agents including spironolactone?

If treatment thresholds are to be driven by estimated CVD risk, at what level should antihypertensive drug treatment be initiated and what other CVD protective agents should be considered?

Is initiating drug therapy with 2 hypertensive agents more effective than initiating with monotherapy for optimal CVD prevention?

Acknowledgments

P.K.W. was supported by P20GM109036 (Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases) from the National Institute of General Medical Sciences.

Footnotes

Competing interests

G.B. served as Consultant for Janssen, Bayer, AbbVie, Vascular Dynamics, Relypsa and Merck; served/serves as Principal Investigator for FIDELIO trial (Bayer), Steering Committee member (CREDENCE)-Janssen, SONAR-AbbVie, and CALM-2-Vascular Dynamics. J.J. served as consultant for Novartis, Novo-Nordisc, Boehringer-Ingelheim, Sanofi, Orexigen, Riemser, Theravance, Vivus; and is cofounder of Eternygen GmbH. S.O. (in the previous 24 months) has received research grant support or reimbursement for travel to meetings or other, non-financial support from Actelion Clinical Research/George Clinical; AstraZeneca AB; Bayer; Lundbeck; Novartis; Novo Nordisk; Rox Medical; has consulted for Actelion/George Clinical, Lundbeck, Novo Nordisk and ROX Medical; served as Director/Principal Investigator, SPRINT University of Alabama at Birmingham (UAB) Clinical Center Network (CCN); and sub-investigator UAB CCN clinical site; for which Takeda and Arbor Pharmaceuticals donated 5% of medication used. N.R.P. served as advisory board member (ad hoc) for Pfizer, Takeda, MSD, Servier, and Medtronic (companies producing blood pressure lowering agents/devices); received speaker honoraria from Servier, AstraZeneca, Napi Labs, and Menarini; received research funding from Servier, Pfizer and Menarini; and is the President of the International Society of Hypertension. George Health Enterprises, the social enterprise arm of The George Institute for Global Health, has applied for a patent in the area of low-dose combinations on which A.R. is listed as an inventor; and has received investment to develop fixed-dose combinations containing aspirin, statin and BP lowering drugs. AR is an investigator on grants for several trials of blood pressure lowering interventions. G.G. has received lectures fees from Merck and Astra Zeneca. M.C.A., R.C., A.F.D., D.R.B. and P.K.W. declare no competing interests.

How to cite this Primer

Publisher's note

References

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Systemic arterial hypertension is the most important modifiable risk factor for all-cause morbidity and mortality worldwide and is associated with increased risk of cardiovascular disease (CVD). Fewer than half of those with hypertension are aware of ...

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En estudio confirmó el papel del sexo masculino como factor de riesgo para el desarrollo de enfermedad cardiovascular en hombres y mujeres hipertensos con cifras comparables de presión arterial.

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Abstract

Aim: The purpose of this study is to study the effect of sex on the features of therapy of arterial hypertension and the development of cardiovascular complications.

Materials and methods: Data from the register of AH from outpatient hospital and cardiology departments of hospitals of 22 regions of the Russian Federation were analyzed. Data of medical documents of 33 564 patients with AH [(36.2%) men and 21 423 (63.8%) women] were entered into the on-line computer program and were analyzed using the statistical software package STATISTICA 10.

Results: Cardiovascular and cerebrovascular diseases are more often diagnosed in men: peripheral artery disease, coronary heart disease, acute coronary syndrome, congestive heart failure, ischemic stroke, dissecting aortic aneurysm. The beginning of development cardiovascular disease in men with elevated blood pressure is already observed at age of 25-44 years, which indicates the need for preventive measures already in adolescence and closer monitoring of treatment at a young age.

Conclusion: The study confirmed the role of the male sex as a risk factor for the development of cardiovascular disease in hypertensive men and women with comparable figures of blood pressure in. Identified gender features must be considered when diagnosing patients with AH.

Keywords: arterial hypertension; cardiovascular complications; cerebrovascular complications; gender differences; registry of arterial hypertension; sex differences.

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Prognostic interactions between cardiovascular risk factors.

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national center for biotechnology information

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Clinical features of arterial hypertension in men and women (according to the National Registry of Arterial Hypertension) - PubMed

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The study confirmed the role of the male sex as a risk factor for the development of cardiovascular disease in hypertensive men and women with comparable figures of blood pressure in. Identified gender features must be considered when diagnosing patients with AH.

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En este estudio se menciona que entre los factores de riesgo modificables están la obesidad, el tabaquismo, alcoholismo, sedentarismo. y entre los factores de riesgo no modificables están los antecedentes familiares, la edad (pacientes geriátricos), el sexo (en hombres son las prevalentes que en as mujeres), y la concurrencia de otras enfermedades como la DM2.

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Factores de riesgo asociados al desarrollo de hipertensión arterial en Chile

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Prevalencia y factores de riesgo asociados de la hipertensión: un estudio transversal en Varanasi urbano

Se encontraron mayores probabilidades de ser hipertenso en sujetos masculinos, grupo de mayor edad, sujetos casados, sujetos de nivel socioeconómico alto, sujetos analfabetos y sujetos jubilados. El consumo de tabaco y alcohol, el sobrepeso, la obesidad y la obesidad abdominal también se asociaron con la hipertensión. Del total de 211 sujetos hipertensos, sólo 81 (38,4%) conocían su estado hipertenso.

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Abstract

Hypertension is a major public health problem and important area of research due to its high prevalence and being major risk factor for cardiovascular diseases and other complications. Objectives. (1) To assess the prevalence of hypertension and its associated factors and (2) to estimate awareness, treatment, and adequacy of control of hypertension among study subjects. Methods and Materials. A community based cross-sectional study with multistage sampling design was conducted among urban population of Varanasi. A modified WHO STEPS interview schedule on 640 study subjects aged 25-64 years was used. Results. The prevalence of hypertension was 32.9% (male: 40.9%, female: 26.0%). Mean systolic and diastolic BP were 124.25 ± 15.05 mmHg and 83.45 ± 9.49 mmHg, respectively. Higher odds of being hypertensive were found in male subjects, eldest age group, married subjects, subjects of upper socioeconomic status, illiterate subjects, and retired subjects. Tobacco and alcohol consumption, overweight, obesity, and abdominal obesity were also associated with hypertension. Out of the total hypertensive 211 subjects, only 81 (38.4%) were aware about their hypertension status; out of those, 57 (70.4%) were seeking treatment and 20 (35.08%) had their blood pressure adequately controlled. Conclusion. Around one-third of the subjects were hypertensive and half of the study subjects were prehypertensive in this area. The awareness, treatment, and control of high blood pressure were also very low.

1. Introduction

Hypertension is a major public health problem due to its high prevalence all around the globe [ 1- 4]. Around 7.5 million deaths or 12.8% of the total of all annual deaths worldwide occur due to high blood pressure [ 5]. It is predicted to be increased to 1.56 billion adults with hypertension in 2025 [ 6].

Raised blood pressure is a major risk factor for chronic heart disease, stroke, and coronary heart disease. Elevated BP is positively correlated to the risk of stroke and coronary heart disease. Other than coronary heart disease and stroke, its complications include heart failure, peripheral vascular disease, renal impairment, retinal hemorrhage, and visual impairment [ 5].

Hypertension (or HTN) or high blood pressure is defined as abnormally high arterial blood pressure. According to the Joint National Committee 7 (JNC7), normal blood pressure is a systolic BP < 120 mmHg and diastolic BP < 80 mm Hg. Hypertension is defined as systolic BP level of ≥140 mmHg and/or diastolic BP level ≥ 90 mmHg. The grey area falling between 120-139 mmHg systolic BP and 80-89 mmHg diastolic BP is defined as "prehypertension" [ 7, 8]. Although prehypertension is not a medical condition in itself, prehypertensive subjects are at more risk of developing HTN [ 1].

It is a silent killer as very rarely any symptom can be seen in its early stages until a severe medical crisis takes place like heart attack, stroke, or chronic kidney disease [ 8- 10]. Since people are unaware of excessive blood pressure, it is only through measurements that detection can be done. Although majority of patients with hypertension remain asymptomatic, some people with HTN report headaches, lightheadedness, vertigo, altered vision, or fainting episode [ 11].

There are several factors predisposing to hypertension. These factors vary from country to country and even there is difference between urban and rural regions of the same place [ 12]. Realizing the effect of urbanization on our collective health, World Health Organization has chosen "Urbanization and Health" as the theme for World Health Day 2010 [ 13]. Urbanization is considered a determinant of health and one of the key drivers of noncommunicable diseases (NCDs), especially in low- and middle-income countries (LMICs) [ 14]. Urban people are more at risk of these diseases as compared to their rural counterparts. As per the findings of National Family Health Survey (NFHS-4), the prevalence of hypertension, obesity, and blood glucose in urban area of Uttar Pradesh was 10.5%, 23.9, and 9.9%, respectively. However, the prevalence of the same phenomenon was 8.3%, 10.8%, and 8.2%, respectively in rural area [ 15]. It is clear that all the parameters are having higher prevalence in urban area as compared to rural area. Rapid urbanization, increasing elderly population, mechanization, sedentary life, and dietary changes act together as a web of risk factors which entangles people in it and leads to several chronic diseases. In order to take effective prevention measures, identification of the risk factors is an essential prerequisite. This study intends to generate information on prevalence of hypertension and their associated risk factors in urban area of Varanasi. In addition, it will also look into the awareness and control of hypertension among the study subjects.

2. Materials and Methods

2.1. Study Area

Varanasi is an Indian city on the bank of Ganges in Uttar Pradesh. It has total population of 3676841 as per Census 2011. As per Census 2011, out of total population, 52% people live in urban areas, while 48% live in the rural areas. There are 90 Census enumeration wards in Varanasi district. Out of these 90 wards, 5 wards were selected by using simple random sampling.

2.2. Study Design and Sample Size

A community based cross-sectional study was carried out among the people aged 25 to 64 years living in the selected study area. The sample size for the present study was calculated by taking most probable prevalence of hypertension as 50% and permissible error as 5% with 95% confidence interval. Fixing the permissible error as 50%, the minimum sample size was calculated as n = 384. Since sampling procedure was multistage, hence considering the design effect, the sample size was further increased by one and half times. Considering the nonresponse rate of 10% the final sample size in study was fixed as 640. In the present study, a prior written informed consent was also taken from the participants. Prior written informed consent was taken by the participants.

2.3. Sampling Methodology

A multistage sampling was used for this study. There were three stages and for each stage different sampling design was used.

At first, out of these 90 wards, 5 wards were selected by using simple random sampling. At second stage, from each selected ward the households were further selected by using systematic random sampling and probability proportional to size was done. At the third stage, one member of target age group was interviewed from selected household. If the selected family has more than one available eligible person then one was chosen randomly by using lottery method. In case of nonavailability of eligible person in a selected household, at the time of survey, the adjacent household was selected.

2.4. Selection of Study Subjects

2.5. Tools of the Study

Interview schedule [modified and pretested WHO stepwise approach to chronic disease risk factor surveillance (STEPS)], Libra weighing machine, steel anthropometry rod, measuring tape, and Omron BP Machine were used.

2.6. Techniques of the Study

In all study participants, a structured and pretested interview schedule was administered to obtain data on sociodemographic parameters.

2.7. Ethical Consideration

Ethical approval was obtained from the Institute Ethical Committee of the Institute of Medical Sciences, Banaras Hindu University Varanasi. Prior written consent was taken from the subjects who volunteered to participate in the study. Identified hypertensive subjects were referred to the nearby clinic for treatment.

2.8. Definitions Used

(i) Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7) classification was used for hypertension [8].

(ii) Hypertension is defined as systolic BP level of ≥140 mmHg and/or diastolic BP level of ≥90 mmHg or being previously diagnosed as hypertensive by any health professional. The area falling between 120-139 mmHg systolic BP and 80-89 mmHg diastolic BP is defined as "prehypertension" [8].

(iii) Isolated diastolic hypertension (IDH) having a systolic blood pressure ≤ 140 mmHg and diastolic blood pressure ≥ 90 mmHg and isolated systolic hypertension (ISH) having a systolic blood pressure ≥ 140 mmHg and diastolic blood pressure < 90 mmHg was used to diagnose IDH and ISH, respectively.

(iv) Awareness was defined as history of hypertension based on diagnosis by a healthcare provider. Treatment was defined as taking any medication or other treatment for hypertension in the last two weeks prior to the survey and control was defined as blood pressure < 140 and <90 mmHg in subjects who were taking medications

(vii) Current daily smokers are defined as those who were currently smoking cigarettes, bidis, or hookah daily. Current daily smokeless tobacco users are defined as those who were currently using chewable tobacco products, gutka, naswar, khaini, or zarda paan daily. Current alcohol drinkers are defined as those who reported to consuming alcohol within the past one year [17].

(viii) Physical activity was measured in three domains that is activity at work, to and from places, and recreational activities as well as time spent sitting. The interview schedule also covered type of activity (vigorous and moderate) at work and for recreational activities. Information was also collected on the number of days in a week spent on different activities and time spent in a day for each activity was also recorded [17]. Those who were not active in any domain were defined as "inactive," those who were vigorously active in any category were defined as "vigorously active," and the rest were "moderately active."

2.9. Data Processing

The information obtained from the survey was entered into a database developed for the study, using SPSS 16.0 program. Descriptive statistics (mean and standard deviation) were calculated for continuous variables and frequencies and percentages were calculated to summarize qualitative data. Other statistical tests like chi-square test and ANOVA were applied. Logistic regression was applied to identify the risk factors for hypertension. A significance level of 0.05 was used.

3. Results

A total of 640 study subjects were interviewed for the survey. Out of these, 301 (47%) were male subjects and 339 (53%) were female. The median age (±SD) of the study subjects was 39.0 (±11.9) years and for male and female it was 40.0 (±11.9) years and 38 (±11.8) years, respectively. Regarding religion and caste of the study subjects, around 96% subjects were Hindu and majority of the subjects were in general category, respectively. Majority of the study subjects were married and one-third of the subjects belonged to the upper socioeconomic class. Mean (±SD) BMI of the study subjects was 24.11 ± 3.94 kg/m ²; for men it was 23.78 ± 3.95 kg/m ² and for women it was 24.41 ± 3.92 kg/m ². According to Body Mass Index (BMI), more than one-third of the study subjects were either overweight or obese. With regard to abdominal obesity as measured by waist circumference, 40% subjects were at risk ().

Table 2

depicts the mean values of systolic and diastolic BP according to age and gender. The mean systolic and diastolic BP of all the study subjects were 124.2 ± 15.0 mmHg and 83.4 ± 9.5 mmHg, respectively. In men, the highest mean systolic BP and mean diastolic BP were among the eldest age group and preceding eldest age group (45-54 years), respectively, while in female the highest mean value of systolic and diastolic BP both were among the 45-54-year age group. With regard to systolic BP, there was significant difference among all the age groups among both male and female study subjects and the same was with diastolic BP as well. The prevalence of isolated systolic BP was found to be 10.6% [95% CI: (8.27-13.37)] and isolated diastolic BP was 19.7% [95% CI: 16.6-23.18]. The proportion was higher in male (14.8%) as compared to female (6.8%). Among both groups (male and female), prevalence was higher among the eldest age group. The prevalence of isolated diastolic BP was higher among male subjects (28.1) against female subjects (12.2%). It was the highest among the second oldest age group among male and oldest age group in female subjects. With regard to systolic BP, age was associated with hypertension status among both genders, whereas diastolic BP was associated with age in male subjects only. There was no association between age and diastolic BP in female subjects.

Table 3

The overall prevalence of hypertension was 32.96% [95% CI: (29.4-36.7)]. The sex specific prevalence was 40.9% [95% CI: 35.5-46.5] for male and 26.0% [95% CI: 21.6-30.9] for female. Prehypertension was prevalent in 45.9% [95% CI: (40.3-51.5)] of men and 38.05% [95% CI: (33.0-43.2)] of women. In men, hypertension was significantly associated with age but in women, age does not have any effect on their hypertension status. History of hypertension or the prediagnosed cases of hypertension was more among female (6.7%) as compared to male (5.9%) subjects ().

Table 4

shows the associated factors of prehypertension and hypertension. Gender, age, marital status, occupation, education status, tobacco use, and physical activity were significantly associated with the hypertension status of the study subjects ( p < 0.05). Both the rate of prehypertension and hypertension were higher among male. Hypertension was more prevalent in the 45-54 years, while prehypertension was more in the 35-44-year age group. Being married and government servant were found to be risk factors for both hypertension and prehypertension. Hypertension was found to be more among illiterate subjects, and with regard to prehypertension, primary educated subjects suffered more. Study subjects from lower and upper socioeconomic status were almost equal victims of hypertension. Tobacco use and alcohol use were found to be risk factors for being hypertensive in the study subjects. Although alcohol use was not significantly associated with hypertension status but rate of hypertension was higher among the alcohol users.

Table 5

The binary logistic regression analysis showed that odds of being hypertensive were higher among the male subjects (OR: 1.97), eldest age group (OR: 6.49), married subjects (OR: 2.34), uneducated subjects (OR: 1.17), retired subjects (OR: 3.66), and those who were from upper socioeconomic status (1.31). With regard to anthropometric risk factors, being overweight (OR: 1.99), being obese (OR: 3.57), and having abdominal obesity (OR: 1.73) had higher odds of hypertension. Tobacco use (OR: 1.86), alcohol use (OR: 1.55), and nonvegetarian diet (OR: 1.10) also had higher odds of being hypertensive. Gender, age, marital status, occupation, BMI, abdominal obesity, and tobacco use were significantly associated with hypertension. Education, socioeconomic status, and alcohol use were not statistically associated with hypertension. Being female, younger in age, unmarried, highly educated, and staying away from any kind of addiction could serve as protective factors against hypertension ().

Table 6

Out of the total subjects with hypertension, around one-third of the subjects were aware of their condition. Out of those who were aware, 70% were seeking treatment. Only a third of the treated subjects with hypertension had their blood pressure adequately controlled (). Females were marginally more aware of their hypertensive status as compared to male counterparts (see , history of hypertension). As age, education status, and socioeconomic status were advancing, the awareness of hypertensive status among study subjects was also increasing (not shown in the table).

4. Discussion

India is a developing country and like other developing countries, it is going through a rapid demographic and epidemiological transition. In all such transitions, nutrition is the key ingredient and plays prime role. This cross-sectional community based study identified a high prevalence of prehypertension and hypertension in urban areas of Varanasi, which was 41.7%   and 32.96%, respectively. Only a quarter of subjects were in the normal category, which highlights the escalating burden of this silent killer.

The prevalence of hypertension in the present study (32.96%) was higher in comparison with the prevalence reported in other studies [ 4, 6, 10, 19- 22]. Few studies reported the results in line with the present study [ 23, 24]. According to World Health Organization (2015), the overall prevalence of hypertension in India was 23.5% and gender specific prevalence was 24.2%  and 22.7% among the men and women, respectively [ 25].

The prevalence of prehypertension in the present study was 41.7% (male: 45.9% and female: 38.05%). The prevalence estimated in the present study was much higher than that estimated by Nellore (22.3%) [ 10] and Bihar (37.95%) [ 20]. The difference of prevalence observed between the present study and other studies with respect to hypertension and prehypertension could be due to social and cultural differences, dietary and lifestyle factors, and also the age span as well as the research methodology used.

Men exhibit higher prevalence of hypertension and prehypertension than their female counterparts (M: 40.9%  and F: 26.0%) and (M: 45.9%  and F: 38.05%), respectively. Similarly, various studies came out with the higher percentage of hypertension in men than women [ 20, 22, 23, 26- 29]. One of the possible explanations for this gender disparity in hypertension prevalence could be partially due to biological sex difference and partially due to behavioral risk factors like smoking, alcohol consumption, or physical activity. We speculate that absentia from alcohol and smoking might be few of those protective factors against hypertension in women. Other than that, women are more interested in health care services utilization and also more frequently report their poor health and therefore they are more likely to have better health [ 6, 30].

Age was found to be an important risk factor for hypertension. As the age was advancing so did the prevalence of hypertension among both the sexes. Similar findings were reported by few other studies also where advancing age was positively related to hypertension [ 1, 6, 19, 21, 22, 26, 31, 32]. With increasing age, the aorta and arteries walls will be stiffened and this contributes to the high prevalence of hypertension in older age groups [ 4].

In the present study, marital status, education, occupation, socioeconomic status, BMI, abdominal obesity, tobacco use, alcohol use, and physical activity were significantly associated with the hypertension.

Low literacy level and being too rich were associated with hypertension. The higher education level was negatively correlated to hypertension in the present study. These studies also supported this finding [ 6, 12, 33]. We speculate that it could be due to the reason that higher education imparts better knowledge and information about hypertension and subsequently those people with higher education had a healthier lifestyle.

revealed that education was significantly associated with hypertension ( χ ² = 17.049, df = 6 and p value = 0.009); however, when adjusted effect of education on hypertension was observed by logistic regression, then no statistical association was observed. Though some studies had shown a significant association of these two variables [ 6, 12], in the study performed in the state of Kerala [ 33], insignificant association between education and hypertension was observed. We speculate that this insignificant association could be due to very few subjects in the illiterate and less educated category. There are so many studies which do not refute the finding of the present study that higher socioeconomic status is a risk for hypertension [ 3, 22, 24, 32, 34- 36]. We assume that better socioeconomic status imparts people with more purchasing power on fast and convenience foods and less physical activity which are already proven to be contributing risk factors for overweight and obesity that subsequently linked to hypertension.

The different anthropometric measurements like BMI, waist circumference, and hip circumference were taken into account to measure overweight, obesity, and central or abdominal obesity. This study showed that overweight and obesity measured by both BMI and waist circumference were major modifiable risk factors to develop hypertension. Overweight subjects had twofold risk of being hypertensive and obese had more than threefold risk for the same in comparison to underweight subjects in this study. There was positive relation observed between increasing BMI and increasing rate of hypertension, which was consistent with other studies [ 1- 4, 6, 12, 20, 21, 23, 32, 36- 39]. South Asians have tendency of developing centralized obesity without developing generalized obesity and because of this waist circumference and waist-hip ratio are better measures of body fat [ 40]. Abdominal obesity (OR: 1.73) also found to be positively linked to high blood pressure in the present study. Various epidemiological and pathophysiological mechanisms explained the link between obesity and hypertension. One of the probable reasons behind this positive relation between obesity and hypertension could be that increased weight increases cardiac output and increased peripheral resistance of arterioles. Other than that, urbanization is also a cause of changes in dietary habits and reduced physical activity which leads to obesity and subsequently results in hypertension [ 4].

Interestingly, we have found inverse association between physical activity and hypertension. Hypertension was more among physically active subjects as compared to inactive subjects (OR: 0.63) but no statistically significant difference was found. Similar result was reported by other study conducted in Turkey [ 1]. The exact reason behind this is unknown and yet to be explored. We speculate that they had started physical activity probably under medical advice after being diagnosed for hypertension or other risk factors like overweight or obesity.

As per WHO report, alcohol consumption was the third largest risk factor in the developed countries and tobacco use was being the second major cause of death worldwide [ 17]. This study indicated the positive association between alcohol and tobacco use and hypertension. Hypertension was more prevalent in tobacco users (OR: 1.86) and alcohol users (OR: 1.55) as compared to nonusers. This finding is supported by other studies also [ 19, 23, 32, 36]. But there are several other studies with contradictory findings [ 1, 21, 41]. Although not statistically significant, odds of being hypertensive were more among nonvegetarian (OR: 1.10) subjects, while vegetarian diet was proved to be protective against hypertension in this study. Several other studies reported the same result [ 3, 19, 33, 34]. A study conducted in Bihar [ 20] refutes this finding and reported that vegetarian diet was positively associated with hypertension.

A recent review study revealed that hypertension awareness rate has been doubled from less than 30% in 1980s to around 60% in present among urban populations and less than 10% in 1980s to 35-40% presently among rural population. However, the treatment and control status is still low at around 30% in urban and 20% in rural areas [ 42]. Rate of awareness, treatment, and control in the present study was observed as 38.4%, 70.4%, and 35.08%, respectively. Previous study conducted in rural Varanasi reported hypertension awareness, treatment, and control (26.5%, 55.6%, and 40%), respectively [ 7].

5. Conclusion & Recommendation

From the results of this study, it can be concluded that the prevalence of both prehypertension and hypertension is very high in urban Varanasi. This makes the people of this area vulnerable to several chronic diseases and other unbearable health consequences. Specifically men are at more risk of being hypertensive than female. Increasing age is proved to be an independent risk factor for hypertension. Programs are needed to improve the surveillance systems and implementation of community based screening programs for early detection of hypertension is also needed. As the awareness of the hypertension status among hypertensive cases was very poor, improving health literacy to increase the awareness of hypertension is also the need of the hour. Interventions like weight management, increased physical activity, increased fruits and vegetables consumption, and reduction in tobacco and alcohol use are required and recommended.

Acknowledgments

The authors would like to thank all the participants for participating in the study.

Additional Points

Limitations of the Study. This study suffers from few of the following limitations. (i) One of the main limitations of this study was the cross-sectional design of the study which restricts examining causal associations. (ii) The study was only conducted in urban areas. (iii) Stress is a major risk factor for hypertension. It could also be considered in the present study for better results.

Conflicts of Interest

There were no conflicts of interest regarding the publication of this article.

References

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Prevalence and Associated Risk Factors of Hypertension: A Cross-Sectional Study in Urban Varanasi

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Hypertension is a major public health problem and important area of research due to its high prevalence and being major risk factor for cardiovascular diseases and other complications. Objectives. (1) To assess the prevalence of hypertension and its associated ...

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Este trabajo define que las causas o el origen de la hipertensión se desconocen así que se asumen en dos tipos: Esencial y secundaria.
Esencial cuando no existe una causa aparente de la hipertensión
Secundaria: Como producto de las manifestaciones clínicas derivadas del padecimiento de otras enfermedades. Según la enfermedad, los mecanismos que contribuyen a la patogenia de la HTA varían desde efectos hormonales sobre la musculatura lisa vascular a cambios en la hemodinámica. En la mayoría de los casos la hipertensión secundaria se debe a enfermedades renales o tiene su origen en trastornos endocrinometabólicos con alteración en la producción de hormonas como la estimulante del tiroides, tiroideas, aldosterona, glucocorticoides o mineralocorticoides.

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La hipertensión es una patología crónica no curable que debe ser sometida a tratamiento de por vida y que es susceptible de provocar alteraciones a medio y largo plazo en función del paciente.

La hipertensión arterial (HTA) constituye el principal riesgo de enfermedad cardiovascular y, por tanto, es una de las principales causas de morbilidad y mortalidad cardiovascular causando graves problemas en la expectativa de vida y en su calidad.

La prevalencia de la HTA varía de forma considerable entre las distintas poblaciones según factores sociales, ambientales y genéticos, pero en general su prevalencia oscila entre el 10 y el 20%. En España, la HTA ocupa el primer lugar en la lista de patologías crónicas en cuanto a motivo de consulta en atención primaria, afectando aproximadamente a un 20% de la población.

No hay una definición clara del concepto de HTA, pero de una forma simple se puede definir como un aumento de la presión arterial por encima de los valores considerados como normales. La definición de hipertensión ha estado influida históricamente por la percepción clínica de la relación entre la presión sanguínea y los efectos derivados que afectan a diferentes órganos del cuerpo humano.

El mayor problema radica en la inexistencia de una clara línea divisoria en los límites de presión arterial que permitan diferenciar individuos normotensos de hipertensos y de cuáles son los valores que deben considerarse factores de riesgo.

En 1984, el Comité Americano para el Control, Evaluación y Tratamiento de la HTA (NJC) propuso una nueva clasificación que es la que se utiliza con mayor frecuencia en la actualidad. Ésta considera normales los valores de presión diastólica inferiores a 85 mmHg, mientras que los comprendidos entre 85 y 90 mmHg también son considerados normales, pero ya son indicativos de alarma.

Los datos señalados con anterioridad se refieren a población normal, pero los valores considerados como normales o patológicos pueden variar en función de diversos estados fisiológicos. La hipertensión gestacional o preeclampsia se caracteriza por un aumento en la presión sistólica mayor o igual a 30 mmHg, y de 15 mmHg en la diastólica con respecto a los valores normales de la paciente antes del embarazo. El hallazgo aislado de un valor elevado de la presión arterial no es indicativo de hipertensión, sino que implica la necesidad de encontrar valores elevados de forma repetida, excepto en el caso de una urgencia hipertensiva.

Clasificación de la hipertensión

La clasificación se puede hacer atendiendo a varios criterios: según el valor de la presión arterial, según el grado de repercusión visceral, según la etiología y según el grado de actividad de renina plasmática.

Según el valor de la presión arterial

Hipertensión arterial diastólica. Leve: 90-104 mmHg; moderada: 105-114 mmHg, y grave: superior a 115 mmHg.

Hipertensión arterial sistólica. Superior a 160 mmHg.

Según el grado de repercusión visceral (OMS, 1978)

Fase I. No aparecen signos objetivos de afectación orgánica.

Fase II. Aparecen uno o más de los siguientes signos: hipertrofia del ventrículo izquierdo, arterias de la retina con estrechez focal o generalizada, proteinuria y/o aumento de la concentración de creatinina en plasma.

Fase III. Se producen los siguientes signos clínicos en diferentes órganos: corazón (insuficiencia ventricular izquierda y a veces angina de pecho e infarto de miocardio), cerebro (hemorragia cerebral, trombosis y encefalopatía hipertensiva), fondo del ojo (hemorragias y exudados retinianos), riñón (insuficiencia renal) y vasos (aneurisma disecante).

Según la etiología

Hipertensión arterial esencial. Cuando no existen causas fisiológicas de origen conocido.

Hipertensión secundaria. Se debe a una gran variedad de causas. Se trata de una manifestación de otra patología. Según la enfermedad, los mecanismos que contribuyen a la patogenia de la HTA varían desde efectos hormonales sobre la musculatura lisa vascular a cambios en la hemodinámica. En la mayoría de los casos la hipertensión secundaria se debe a enfermedades renales o tiene su origen en trastornos endocrinometabólicos con alteración en la producción de hormonas como la estimulante del tiroides, tiroideas, aldosterona, glucocorticoides o mineralocorticoides.

Según el grado de actividad de renina plasmática

HTA con actividad de renina plasmástica baja.

HTA con actividad de renina plasmática normal.

HTA con actividad de renina plasmática elevada.

Patogenia de la hipertensión

La HTA puede ser debida a diversas causas y multitud de factores se han relacionado con la patogenia y agravamiento de la hipertensión. A la hora de clasificar la HTA desde un punto de vista etiológico, a grandes rasgos se puede hablar de HTA renal, endocrina, genética, neurogénica y pendiente de renina.

Hipertensión renal

Las alteraciones en la hemodinámica intrarrenal contribuyen a la patogenia de la HTA, y cualquier oclusión en las arterias renales produce un aumento en la presión arterial. La nefroesclerosis, la glomerulonefritis, la nefropatía diabética, infartos renales, trombosis renales, tumores, etc. pueden provocar HTA.

Otro mecanismo por el cual la enfermedad renal posee un papel en la patogenia de la hipertensión está relacionado con la capacidad que tiene el riñón para excretar sal y agua. Un aumento en la retención de sodio y líquidos produce un incremento de la presión arterial.

Hipertensión endocrina

La aldosterona provoca HTA como consecuencia de un aumento en la retención de sodio. Esta hormona es secretada por la zona glomerular de la corteza suprarrenal, y en el aldosteronismo primario la velocidad de secreción aumenta y se vuelve autónoma. La hipertensión resultante es consecuencia del aumento en la retención de sodio y en el volumen plasmático.

Los esteroides también poseen un efecto mineralocorticoide, por lo que en el síndrome de Cushing es característica la HTA. También la hiperplasia renal congénita se acompaña de un exceso de mineralocorticoides e hipertensión.

Hipertensión genética

Los sujetos procedentes de progenitores con HTA padecen la enfermedad con mayor frecuencia que aquellos cuyos padres no la padecieron, demostrándose que la hipertensión puede tener una base genética. En la actualidad ya es un hecho, constatado mediante estudios epidemiológicos, que existe una mayor incidencia de la HTA en familiares de sujetos con la patología establecida, fenómeno denominado como "agrupación familiar".

Hipertensión neurogénica

En las regiones laterales y posteriores del hipotálamo hay centros presores que producen aumentos agudos de la presión arterial, por lo que la lesión cerebral de estructuras que controlan la actividad simpática puede inducir HTA crónica.

El sistema nervioso constituye el mecanismo de control más rápido de la presión. Un aumento de la actividad nerviosa simpática modifica la liberación de renina y de aldosterona, alterando la capacidad renal para excretar sodio y agua, al mismo tiempo que provoca vasoconstricción arteriolar.

Hipertensión dependiente de renina

El sistema renina-angiotensina-aldosterona puede participar en la patogenia de la HTA. La angiotensina II se forma a partir de la angiotensina I por acción de la enzima de conversión de la angiotensina (ECA), siendo un potente vasoconstrictor. Además, la ECA inhibe la formación de cininas, que actúan como sustancias vasodilatadoras.

Riesgos derivados de la HTA

Mortalidad

La importancia que la hipertensión tiene sobre la mortalidad por problemas cardiovasculares es difícil de valorar. Mediante estudios epidemiológicos se observó una relación directa entre hipertensión y mortalidad, incrementándose el riesgo a medida que lo hace la hipertensión. Si se valora el índice de mortalidad por accidentes vasculares cerebrales, cuyo principal desencadenante es la HTA, se llega a idénticas conclusiones. Cuanto antes aparece la HTA menor es la expectativa de vida.

Enfermedad cardiovascular

No cabe duda de que la HTA está reconocida como el mayor factor de riesgo en todo tipo de patologías cardiovasculares, incluida la insuficiencia cardíaca, la cardiopatía isquémica y las enfermedades periféricas vasculares. La incidencia de infarto de miocardio y de enfermedad coronaria es mucho mayor en la población hipertensa que en la normotensa, por lo que la HTA constituye una de las principales causas de muerte cardíaca.

El estudio de la función ventricular izquierda del enfermo hipertenso es de gran interés para estimar el pronóstico evolutivo de la HTA y valorar la terapia a emplear. El sistema cardiovascular se debe adaptar a la sobrecarga funcional, pudiendo aparecer:

Insuficencia cardíaca. La HTA aguda puede ocasionar insuficiencia cardíaca global debido a una sobrecarga mecánica que hace que el corazón sea incapaz de responder a las necesidades metabólicas del organismo. Aparece palidez, disnea, ortopnea, ritmo de galope, sudación, tercer o cuarto tono, cirrosis y distensión en las venas del cuello. En respuesta al aumento de la poscarga, el organismo debe adaptarse a la situación hipertensiva mediante una serie de pasos compensatorios como el aumento de la tasa de filtración glomerular y diuresis, el aumento de la presión de perfusión coronaria y del flujo a través de las arterias, o la reducción en el tono simpático.

Insuficiencia miocárdica sistólica y diastólica. Se altera la cinética del calcio intracelular, con un incremento en las concentraciones de este ión en el interior de las mitocondrias que puede provocar insuficiencia miocárdica sistólica debida a alteraciones en el inotropismo. La disminución de la concentración de calcio en el exterior de las células por desplazamiento anormal hacia el interior de las mitocondrias produce una mayor relajación ventricular que lleva a una insuficiencia miocárdica diastólica.

Arteriolitis. El sistema vascular está compuesto de pequeñas arterias que poseen elasticidad y capacidad contráctil, siendo capaces de regular el tono circulatorio. Durante el estado de hipertensión sostenida las arterias sufren cambios en su distensibilidad, que depende mucho de su calibre.

El aumento de la presión arterial provoca anomalías en la contractibilidad de la musculatura vascular, originando zonas de sobredistensión que provocan turbulencias lesivas sobre la pared. Se produce degeneración de la pared arteriolar, necrosis tisular y estenosis luminal progresiva.

Cuando la HTA es leve, se produce un depósito de material hialino que difunde a las distintas capas del vaso, y con el paso del tiempo tiende a formar colágeno, lo que lleva a la arteriosclerosis hialina. En caso de tratarse de HTA grave las lesiones dependen mucho del calibre del vaso, pero en general son de mayor importancia. Debido a la respuesta adaptativa al incremento de la presión arterial, se produce una cicatrización de los depósitos de fibrinioides que emigran hacia la íntima por fenestraciones de la lámina interna, produciéndose un engrosamiento concéntrico de los vasos con depósitos hialinos focales; es lo que se conoce como arteriolitis hiperplásica.

En el riñón, la HTA produce nefroangiosclerosis. En los estadios iniciales coexisten glomérulos normales con lesionados. Éstos muestran aspecto isquémico con engrosamiento de las paredes capilares. Los glomérulos isquémicos se contraen de forma progresiva y la cápsula de Bowman sufre un depósito de colágeno intracapsular en su cara interna. A medida que la lesión progresa se convierte en nefrosclerosis maligna y aparecen hemorragias capsulares, se forman gotas lipídicas y los glomérulos muestran separaciones entre el endotelio y la membrana basal, con depósitos de fibrina. Se acompaña de un cuadro de hematuria, proteinuria e insuficiencia renal, pudiendo llegar a la anuria.

Globo ocular

Aparecen una serie de lesiones oculares relacionadas con el grado de hipertensión. Se produce un estrechamiento generalizado de las arteriolas. En principio aparece un brillo de las arteriolas, que sufren una ligera depresión marcando las partes del estrechamiento. Cada vez sufren una depresión más clara y se habla de arteriolas en hilo de cobre. Cuando ya es muy avanzada aparecen cambios en el trayecto de las venas, que se denominan "en hilo de plata".

El aumento de la presión arterial provoca anomalías en la contractibilidad de la musculatura vascular, originando zonas de sobredistensión que provocan turbulencias lesivas sobre la pared

Pueden presentarse hemorragias y exudados que se clasifican en función del número de cuadrantes que afectan. Cuando la hipertensión es de predominio diastólico se produce una vasoconstricción segmentaria, disminuyendo el calibre arteriolar y perdiéndose la relación arteria/vena; con el tiempo aparecen lesiones como hemorragias, accidentes vasculares e infiltrados de lípidos. Cuando fracasa la perfusión retiniana se necrotiza la arteriola terminal.

Una de las mayores complicaciones de la HTA son los accidentes cerebrovasculares. El aumento de la presión arterial puede provocar hemorragias cerebrales y, en presencia de aterosclerosis, trombosis. También son frecuentes las encefalopatías hipertensivas, que es un síndrome neurológico caracterizado por cefaleas, somnolencia, vértigo, confusión y, en último termino, convulsiones y un estado de coma.

Entre los accidentes cerebrovasculares destacan los siguientes:

Hemorragias subaracnoideas. Se produce una rotura del aneurisma que provoca cefalea intensa, rigidez de la nuca y ausencia de signos neurológicos focales.

Hemorragias intraparenquimatosas. Ocasiona una intensa cefalea, náuseas, vómitos y defectos sensoriales. Las alteraciones neurológicas dependen de la localización, siendo las talámicas las que presentan un pronóstico más complicado, mientras que las pontianas producen cuadriparesia y un coma profundo.

Factores que alteran la HTA

Una vez establecido el diagnóstico de hipertensión, se debe llevar a cabo un tratamiento no farmacológico y aplicarlo a todos los sujetos, con independencia de que éste pueda ser suficiente o sea necesario añadir una terapia farmacológica. Dicho tratamiento se basa en reducir el consumo de ciertas sustancias y modificar algunos hábitos de vida.

Peso corporal

La HTA desciende con la pérdida de peso derivada de la restricción calórica mediante dietas con bajo contenido en grasas. Asimismo, se recomienda aumentar el consumo de fibras y disminuir el de alimentos de origen animal. Con ello se reducen los niveles de colesterol total y aumenta la fracción HDL; pero estos pacientes vuelven a los niveles previos de HTA tan pronto como abandonan el régimen y recuperan el peso perdido.

Existe una relación entre hipertensión y obesidad, siendo ésta un factor predictivo de la HTA, aunque sobre ambos factores influye el componente genético. Por eso, la reducción del sobrepeso en ocasiones es suficiente para controlar la HTA, y además se evita la sobrecarga del corazón y la aparición de diabetes e hiperlipemia.

Para lograr una mayor efectividad es aconsejable que una dieta pobre en calorías se acompañe de ejercicio físico que, además de ayudar a controlar el peso, produce una disminución de la resistencia vascular periférica.

Una de las mayores incógnitas es la relación real existente entre el consumo de sal y los niveles de HTA. Uno de los datos más curiosos surge en países o zonas con un consumo de sal muy bajo o casi nulo, donde se ha observado que los habitantes raramente padecen hipertensión; pero a medida que éstos emigran a sociedades industrializadas, la incidencia de hipertensión aumenta igual que lo hace el consumo de sal. En la actualidad hay diversos estudios que demuestran la relación cuantitativa directa entre el consumo de sal y la HTA. En países con dietas bajas en sodio es poco frecuente la hipertensión, mientras que en países con gran consumo de sal la incidencia es mayor.

No hay duda de la conveniencia de limitar el consumo de sal en todos los sujetos hipertensos, pero hay que tener en cuenta que el 40% de éstos son lo que podríamos llamar "salrresistentes", por lo que esta medida no modifica los niveles de presión sanguínea.

Sin embargo, en los demás casos la reducción de la ingesta de sodio es a veces ya suficiente para controlar la HTA sin necesidad de recurrir a tratamientos farmacológicos. Hay que recordar que la reducción no debe ser drástica, ya que se pueden producir depleciones salinas que pueden favorecer la hipotensión ortostática.

El sujeto hipertenso no debe consumir más de 5 g al día de sal, reduciendo ésta como condimento de cocina y no consumiendo aquellos alimentos que ya son ricos en sal.

Un sujeto hipertenso no debe sobrepasar los 300 mg de cafeína por día (aproximadamente unas 3 tazas). La cafeína es un excitante que produce taquicardia y un aumento en la resistencia vascular cerebral, siendo capaz de elevar la presión arterial sistólica de forma transitoria, aunque carezca de efectos a largo plazo o sobre la prevalencia de la HTA en la población.

En general, parece aconsejable limitar el consumo de alcohol a los 30 g diarios y no sobrepasar los 80. Se cree que el consumo excesivo de alcohol aumenta la HTA y altera la eficacia de las medidas terapéuticas aplicadas, aunque no existe acuerdo general sobre esta relación cuando el consumo es moderado, e incluso parece que puede resultar beneficioso para el flujo coronario.

Se ha encontrado una correlación positiva entre el consumo de alcohol y la aparición de hemorragias cerebrales que están ligadas a hipertensión, pero, por otra parte, la relación es inversa cuando se relaciona el alcohol con la frecuencia de cardiopatías trombóticas.

No ha podido comprobarse una relación directa entre el consumo de tabaco y la elevación de la presión sanguínea, aunque sí se ha establecido con el riesgo de padecer enfermedad cardiovascular, por lo que el tabaco también debe ser tomado en consideración.

Aunque en algunos casos la población fumadora tiene unos valores de HTA inferiores a los de la no fumadora, este hecho probablemente se debe a una reducción del peso corporal, parámetro que incide directamente en la presión sanguínea. En cualquier caso, las innumerables repercusiones cardiovasculares desfavorables hacen recomendable reducir o suprimir el consumo de tabaco.

El tabaco, además, disminuye la eficacia de algunos fármacos antihipertensivos, aumenta el colesterol total y los triglicéridos y afecta de forma negativa a la circulación sanguínea y a la hemostasia.

Existe una relación entre hipertensión y obesidad, siendo ésta un factor predictivo de la HTA, aunque
sobre ambos factores influye el componente genético

Estilo de vida

Los problemas psicológicos y el estrés favorecen la hipertensión, por lo cual se debe intentar llevar una vida relajada. Por otra parte, el sedentarismo facilita la obesidad, que es uno de los principales factores de riesgo en el desarrollo de la hipertensión, mientras que el ejercicio físico practicado de forma habitual y moderada ayuda a controlar el peso corporal y favorece la relajación.

Medidas dietéticas

Se sugiere que puede haber una correlación inversa entre la ingesta de potasio y la HTA. El exceso de sodio produce menos efectos sobre la presión si éste se administra con potasio, debido a que aumenta la excreción de sodio por el riñón. Algunos investigadores también consideran que el calcio puede afectar a la presión arterial, pero hay datos que apoyan distintas teorías y es difícil extraer conclusiones. Si se confirma su influencia, sería recomendable tenerlo en consideración, sobre todo al analizar la dureza de las aguas. *

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# data[].attributes.attachment_link.title
Etiología y riesgos de la hipertensión | Offarm

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La hipertensión es una patología crónica no curable que debe ser sometida a tratamiento de por vida y que es susceptible de provocar alteraciones a medio y largo plazo en función del paciente.

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Los factores de riesgo asociados a la hipertensión arterial fueron la baja escolaridad, el tabaquismo prolongado, el peso corporal excesivo y la obesidad.

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Affiliation

¹ Institute of Epidemiology, 2Institute of Social Medicine; Medical School, University of Belgrade, 3Primary Health Centre ''Stari Grad", 4City Institute for Skin and Venereal Diseases; Belgrade, Serbia.

Affiliation

¹ Institute of Epidemiology, 2Institute of Social Medicine; Medical School, University of Belgrade, 3Primary Health Centre ''Stari Grad", 4City Institute for Skin and Venereal Diseases; Belgrade, Serbia.

Abstract

Aim: To examine risk factors for the development of primary arterial hypertension which is a significant health and public health problem throughout the world.

Methods: This anamnestic study, conducted at the Primary Health Centre "Stari Grad" in Belgrade during 2006, included 63 new cases of arterial hypertension and 63 subjects who formed the control group. Patients and control group were individually matched to each other by sex, age (+/- 3 years) and place of residence. The survey instrument was a questionnaire based on socio-demographic characteristics of respondents (gender, age, residence, education level, occupation, marital status, socio-economic status) and habits (smoking, alcohol consumption, physical activity). Data analysis was performed by applying descriptive statistics (relative numbers) and inferential statistics (χ2 test).

Results: There were significant differences in the level of education (p = 0,012) and current smoking status (p=0.017) between the group of patients with arterial hypertension and the control group. The subjects in the control group showed significantly longer consumption of schnapps (p=0.033) and beer (p=0.040) (more than 20 years). There was a significant difference in excessive body weight, and obesity measured by body mass index (p=0.006) and waist circumference (p=0.014) between these groups of patients.

Conclusion: Risk factors associated with arterial hypertension were low education, long smoking period, excessive body weight and obesity. These results indicate the necessity of introducing programs which should be imperative in future prevention of arterial hypertension.

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national center for biotechnology information

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Risk factors for the development of arterial hypertension - PubMed

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1 Institute of Epidemiology, 2Institute of Social Medicine; Medical School, University of Belgrade, 3Primary Health Centre ''Stari Grad", 4City Institute for Skin and Venereal Diseases; Belgrade, Serbia. 1 Institute of Epidemiology, 2Institute of Social Medicine; Medical School, University of Belgrade, 3Primary Health Centre ''Stari Grad", 4City Institute for Skin and Venereal Diseases; Belgrade, Serbia.

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La epidemiología de la hipertensión arterial en el Perú ha sido preocupación permanente de los investigadores peruanos, los que han realizado múltiples estudios en las distintas ciudades del país, con resultados variados, diferentes e inconsistentes, por haberse realizado en lugares y en grupos poblacionales distintos, aplicando metodología y criterios de definición diversos.

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Citado por SciELO

Similares en SciELO

SIMPOSIO: HIPERTENSIÓN ARTERIAL

Epidemiología de la Hipertensión Arterial en el Perú
Epidemiology of Arterial Hypertension in Peru
1 Médico Cardiólogo. Profesor Emérito, Universidad Peruana Cayetano Heredia. Ex Presidente de la Sociedad Peruana de Cardiología

Objetivos: Determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en el Perú. Diseño, lugar, participantes: Aplicación de encuesta y medida de presión arterial a población adulta de ambos sexos, mayores de 18 años en 26 ciudades, 10 en la costa, 4 en la selva y 12 en la sierra, localizadas a diferentes alturas a nivel del mar. En la sierra, fueron agrupadas por su altitud en menos y más de 3000 msnm. En total, quedaron 14 256 encuestas válidas. Intervenciones: La obtención de la muestra se realizó entre febrero y noviembre de 2004. La presión arterial fue obtenida con los mismos tensiómetros, de acuerdo a las recomendaciones establecidas. Para el diagnóstico de la presión arterial, se utilizó el criterio del VII Comité Nacional Conjunto. Resultados: La prevalencia de hipertensión en la población general fue 23,7% (varones 13,4% y mujeres 10,3%). En la costa, la prevalencia fue 27,3%; en la sierra 18,8% y 22,1% en las altitudes menores y mayores de 3000 msnm, respectivamente; en la selva, 22,7%. A partir de la cuarta década de la vida, la posibilidad de desarrollar hipertensión fue mayor en la costa que en las otras regiones. Los hipertensos diastólicos fueron predominantes en la sierra, sobre los 3 000 msnm; 55% de la población no sabía que era hipertenso; de quienes recibían tratamiento, solo 45,1% estaba compensado; la mayoría (82,2%) recibía tratamiento con los inhibidores de la enzima convertidora de la angiotensina (ECA) I. Se especula teorías en relación al hematocrito, vasodilatación e hipervascularización. Conclusiones: La hipertensión es casi similar en las tres regiones del Perú. A partir de la cuarta década de la vida, la posibilidad de desarrollar hipertensión es mayor en la costa. Los hipertensos diastólicos fueron predominantes en la sierra, sobre los 3 000 msnm; más de la mitad de la población no sabía que era hipertenso y, de quienes recibían tratamiento, solo 45,1% estaba compensado; la gran mayoría recibía tratamiento con los inhibidores específicos de la enzima convertidora de la angiotensina (ECA) I.

PALABRAS CLAVES: Hipertensión arterial, epidemiología, Perú, diagnóstico, costa, sierra, selva.

Objective: To determine arterial hypertension prevalence, knowledge, treatment, and control, in Peru. Design, setting, participants: Cross sectional survey application and blood pressure measurement performed in 26 cities in 18 year-old or over adult population, 10 cities in the coast, 12 in the mountains at different altitude (below and above 3 000 meters above sea level), and 4 in the jungle. Interventions: The study done between February and November 2004 considered valid 14 256 surveys. Blood pressure was obtained with the same standard equipment, and diagnosis followed the recommendations of the Joint National Committee's Seventh Report. Results: Arterial hypertension prevalence was 23,7% (males, 13,4%; females, 10,3%). In the coast, the prevalence was 27,3%; in the mountains, 18,8% below 3 000 meters and 22,1% above 3 000 meters; in the jungle, 22,7%. After the fourth decade of life the possibility of developing hipertensión was higher in the coast than in the other regions of Peru. Diastolic hypertension was predominant above 3 000 meters. The study determined that 55% of the population did not know they had hypertension; from those under treatment, 45,1% were compensated; 82% received angiotensin converting enzyme I inhibitors. We speculate on hematocrit, vasodilation and hypervascularization theories. Conclusions: Hypertension prevalence was similar in the three Peruvian regions. The possibility of developing hypertension after the fourth decade of life was higher in the coast. Diastolic hypertension was predominant above 3 000 meters. Over one half of the population did not know they had hypertension; from those Ander treatment 45,1% were compensated; most of the patients received angiotensin converting enzyme I inhibitors.

Keywords: Arterial hypertension, epidemiology, Peru, diagnosis

La hipertensión arterial es uno de los factores de riesgo modificable de mayor prevalencia en el mundo. Participa en el desarrollo de la enfermedad aterosclerótica cardiovascular, en la morbimortalidad por eventos cardiacos, cerebrovasculares, insuficiencia renal y enfermedad vascular periférica, como riesgo continuo sin evidencia de umbral, hasta por debajo de 115/75 mmHg, por lo que la expectativa de vida de estos pacientes se encuentra reducida1.

La epidemiología de la hipertensión arterial en el Perú ha sido preocupación permanente de los investigadores peruanos, los que han realizado múltiples estudios en las distintas ciudades del país, con resultados variados, diferentes e inconsistentes, por haberse realizado en lugares y en grupos poblacionales distintos, aplicando metodología y criterios de definición diversos.

La hipertensión arterial ha sufrido cambios en su definición, de acuerdo a los sucesivos Reportes del Comité Nacional Conjunto, tanto en Estados Unidos como en Europa, criterios que son aplicados en la mayoría de los estudios epidemiológicos del mundo.

El Perú es un país geográficamente accidentado, con sus tres regiones costa, sierra y selva. En la sierra, las ciudades están situadas a diferentes alturas sobre el nivel del mar. En cada región, las costumbres de trabajo, alimentación, educación y cultura son diferentes, lo que influye en los factores de riesgo cardiovascular y probablemente en el desarrollo de la aterosclerosis.

Al componente socio cultural y al incremento de la población habría que agregar los cambios biológicos por la altura y la predisposición genética.

En el Perú, en las últimas décadas han acontecido importantes cambios en la distribución de la población, con un incremento acelerado, básicamente por una gran migración del campo a la ciudad, de la región andina a la costa, de rural y agrícola a grandes concentraciones urbanas, en busca de mejores niveles de vida.

La hipertensión arterial disminuye la calidad de vida y la supervivencia de la población, por lo que es un reto importante para la salud pública. Para un tratamiento adecuado, es necesario determinar la prevalencia, el tratamiento y control de la hipertensión arterial en las diferentes ciudades en las 3 regiones del país, lo que permitirá conocer la realidad nacional y poder aplicar la prevención, método importante y económico difundido en todo el mundo, responsabilidad que pertenece a los organismos de Salud Pública del Estado.

Presentamos los resultados del estudio de la prevalencia de la hipertensión arterial en el Perú realizado de febrero a noviembre de 2004, en 26 ciudades del país, distribuidas en costa, sierra y selva.

Para la recolección de los datos, se utilizó el protocolo diseñado para determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en la población adulta de ambos sexos, mayores de 18 años, en 26 ciudades del país, 10 ciudades en la costa, 12 en la sierra y 4 en la selva. En la sierra, las ciudades están localizadas a diferentes alturas sobre el nivel del mar. La obtención de la muestra se realizó de febrero a noviembre de 2004. Se realizó 14 826 encuestas en las 26 ciudades; se excluyó del análisis 538 encuestas, vueltas a realizar en la ciudad del Callao y que fueron utilizadas como control de calidad. Además, se excluyó 32 encuestas, por presentar datos inconclusos o recogidos inadecuadamente, quedando 14 256 encuestas válidas. La presión arterial fue obtenida utilizando los mismos 19 tensiómetros de mercurio calibrados en Lima y luego transportados por las monitoras, enfermeras licenciadas en investigación, a las diversas ciudades, de acuerdo con un cronograma previamente determinado. En cada ciudad, se nombró un investigador principal, miembro de la Filial de la Sociedad Peruana de Cardiología y, en los lugares donde no había filial, se nombró un médico de la ciudad de reconocido prestigio. Los investigadores principales fueron reunidos en Lima en dos etapas, con los que se realizó seminarios-talleres para unificar criterios, la forma de obtener los datos, llenar las encuestas y el método adecuado de la toma de la presión arterial, ilustrados con videos que fueron proporcionados para las sedes respectivas.

Cada investigador, en su sede, nombró a los investigadores secundarios y a las encuestadoras, que podían ser médicos, estudiantes de medicina y enfermeras, todos calificados y con experiencia. El día previo a la encuesta, la monitora reunía y entrenaba a los participantes en la obtención de los datos y la toma de la presión arterial. Las encuestas fueron realizadas en lugares públicos, parques y otros lugares concurridos, alejados de los hospitales, centros de salud y postas médicas. La presión arterial fue obtenida al final de la encuesta, mientras la persona permanecía sentada y en reposo, en el miembro superior derecho, de acuerdo a las recomendaciones del Sétimo Comité Nacional Conjunto ². Las encuestas originales quedaron archivadas en la ciudad del lugar de la obtención y la copia en la Oficina Central de la Sociedad Peruana de Cardiología. Después de depurar los datos obtenidos, se realizó los cálculos estadísticos de la prevalencia de la población total del Perú, por ciudades aisladas y luego las ciudades por región natural, costa, sierra y selva. Luego, las ciudades de la sierra fueron agrupadas por su altitud, en menos y más de 3 000 msnm, consideradas medianas y grandes alturas, respectivamente.

Para el diagnóstico de la presión arterial, se utilizó el mismo criterio del Sétimo Comité Nacional Conjunto (2004), que considera normal < 120/80 mmHg; prehipertensión, < 139/89 mmHg; hipertensión arterial grado I > 140/90 mmHg y grado II, > 160/90 mmHg. Se consideró también hipertensas a las personas que tenían diagnóstico previo por un profesional médico y personas que tenían tratamiento para hipertensión arterial. Se consideró control farmacológico de la hipertensión arterial cuando con el tratamiento hipotensor se encontró presión arterial sistólica menor de 140 mm de Hg y diastólica menor de 90 mm de Hg.

Se obtuvo 14 256 encuestas en 26 ciudades del Perú, localizadas en la costa, sierra y selva. En la sierra, las ciudades están situadas a diferentes alturas sobre el nivel del mar.

El 50,8% de la población total correspondió a varones y 49,2% a mujeres, con un promedio de edad de 43,5 años para varones y 40,7 años para mujeres. En el análisis de la distribución de la población, se encuentra la mayoría de los encuestados en las primeras décadas de la vida, para disminuir progresivamente hacia las últimas décadas, con hallazgo similar en ambos sexos y en las tres regiones del país ( Tabla 1).

La prevalencia de la hipertensión arterial en la población general del Perú fue de 23,7%, en mayores de 18 años, lo que correspondería a 3 650 000 habitantes, estimado en base al censo 2005, con un predominio de hipertensos varones de 13,4% sobre hipertensas mujeres de 10,3%. Predominio de sexo masculino que persiste en los hipertensos de la costa, sierra y selva.

La prevalencia de la hipertensión arterial por sexo, de toda la población, fue 27,1% en varones y 20,4% en mujeres ( Tabla 2).

En toda la población y en las tres regiones, la prevalencia de la hipertensión arterial se incrementó progresivamente con la edad en ambos sexos, con predominio de la costa hasta la década de los sesenta, cuando aparecieron algunos cambios. En la sierra, dicha prevalencia declinó y aumentó en la selva, con relación a la costa. Estos resultados indicarían que, la probabilidad de desarrollar hipertensión arterial a partir de la cuarta década de vida, siempre es mayor en la costa que en la selva y menor aún en la sierra, a iguales edades, por influencia de probables factores que discutiremos posteriormente. ( Figura 1)

La hipertensión arterial sistólica es predominante en las primeras décadas de la vida, para luego decaer progresivamente, un comportamiento diferente al de las hipertensiones diastólica y sistodiastólica. Figura 2.

La prevalencia de la hipertensión arterial en la costa fue 27,3%, en la sierra 20,4% y en la selva 22,7%. En la sierra, al separar las ciudades cuya altura era por debajo de 3 000 msnm (metros sobre el nivel del mar) la prevalencia fue 18,8%, en las ciudades de menor altura, y sobre 3 000 msnm, la prevalencia fue mayor, 22,1%, hallazgo de gran importancia, que será analizado en la discusión. En las cuatro regiones, hay predominio del sexo masculino ( Figura 3).

Las ciudades con mayor y menor prevalencia en el país fueron: el Callao, con 34,5%, y Abancay, con 12,4%, respectivamente, como se observa en la figura 4, en ella se dispone las ciudades en relación a las tres regiones del país.

En todas las ciudades, la hipertensión arterial fue de mayor prevalencia en el sexo masculino; excepto en Chachapoyas, Cajamarca, Cerro de Pasco y el Callao, donde este predominio no es significativo.

La prevalencia de la hipertensión arterial en las ciudades de la altura no mostró una relación directa de mayor altitud a menor prevalencia de la hipertensión arterial; los resultados fueron variables. Las ciudades de la sierra con mayor prevalencia fueron Chachapoyas, Arequipa, Huaraz y Puno y, las de menor prevalencia, Huánuco y Abancay, ciudades situadas en la sierra, por debajo de los 3 000 msnm. Figura 4.

Analizando los resultados del VII Report, que define presión normal o ideal, prehipertensión, hipertensión estadio I y estadio II. En toda la población, la hipertensión arterial estadio I (17,9%) fue de mayor prevalencia que el estadio II (5,8%), que es de mayor severidad y con predominio del sexo masculino en ambos estadios. La presión arterial normal y la prehipertensión (considerados normales) fueron siempre de mayor prevalencia en las mujeres y hombres respectivamente ( Tabla 3).

Con relación a la altura sobre el nivel del mar, la presión arterial normal (ideal) fue siempre de mayor presentación en la sierra 'media' (49,7%) y 'alta' (45,3%) y en la selva (44,4%), en comparación a los resultados de la costa (37,1%). Mientras que, el estadio prehipertensión fue de presentación similar en las cuatro regiones del país.

La prevalencia en ambos estadios I y II fue siempre menor en la sierra y selva, en comparación a la costa. Un hallazgo importante fue encontrar que la prevalencia de la hipertensión arterial en las ciudades con altitud sobre 3000 msnm es ligeramente mayor que la prevalencia de las ciudades de altura por debajo de 3000 msnm ( Figura 5).

Los hipertensos diastólicos fueron siempre predominantes en la sierra situada sobre los 3 000 msnm. Figura 6.

Analizando la distribución de los hipertensos de acuerdo al "conocimiento de su condición de hipertensos, tratamiento y control" se encuentra que del total de la población de hipertensos 55,1% no sabían que eran hipertensos, y quienes sí conocían su condición de hipertensos fueron 44,9%.

De los que conocían que eran hipertensos, 72,7% recibía diferente tratamiento, 18,9% farmacológico, 4,6% dietético, 9,2% tratamiento farmacológico y dietético y 12,2% ningún tratamiento. Lo más saltante de quienes recibían tratamiento, solo 45,1% estaban compensados y la mayoría, 54,9%, era hipertenso no compensado. Esto demuestra la ineficacia del tratamiento que se presenta en ambos sexos y en las tres regiones del país en donde el 64,6% de los hombres y 42,6% de las mujeres ignoraban su condición de hipertensos. En el análisis de las tres regiones, el mayor desconocimiento fue en la sierra (59,9%), luego en la selva (57%) y en la Costa (51%). El desconocimiento de su hipertensión arterial fue siempre mayor en los hombres en la sierra y selva, mientras que en la costa el desconocimiento fue similar tanto en hombres como en mujeres ( Figura 7).

Los resultados del tratamiento farmacológico que recibían los hipertensos muestran que la gran mayoría (82,2%) recibía inhibidores de la enzima convertidora, seguidos por los calcioantagonistas dihidropiridínicos (12%) y luego otros hipotensores. ( Tabla 4).

Este esquema terapéutico se repite en las tres regiones del país.

Esta encuesta representa el estudio epidemiológico más grande sobre la prevalencia de la hipertensión arterial (HTA) y de otros factores de riesgo cardiovascular realizados en el Perú. Comprende 26 ciudades de las tres regiones de país: costa, sierra y selva. Las ciudades de la sierra se encuentran situadas a diferentes alturas sobre el nivel del mar. La preparación previa del personal médico y paramédico para la obtención de los datos de la encuesta y la toma de la presión arterial de acuerdo a la buena practica clínica, el uso de los mismos tensiómetros de mercurio en todas las ciudades, permitió tener datos más exactos y precisos sobre la detección, tratamiento y control de la hipertensión arterial en la población general. El análisis de la distribución por edad y sexo, de la población encuestada, fue similar en todas las regiones del Perú. La mayor población corresponde a las primeras décadas de la vida y luego disminuye progresivamente hasta las últimas décadas, lo que indica la obtención adecuada de la muestra.

Los datos obtenidos de este estudio deben ser tomados en forma relativa, al comararlos con estudios epidemiológicos nacionales e internacionales previos; los que fueron realizados utilizando diferentes variables y el empleo de diferentes definiciones de hipertensión arterial3-35.

En el presente estudio, se utilizó los criterios del VII Comité Nacional Conjunto del 20042.
De acuerdo a los resultados, 23,7% de la población mayor de 18 años en el Perú, tiene hipertensión arterial, que representa alrededor de 3 650 000 habitantes, población basada en el último censo de 2004. En las tres regiones del país, se encontró una mayor prevalencia de hipertensos en el sexo masculino (13,4%) sobre el sexo femenino (10,3%), lo que está de acuerdo con estudios nacionales previos.

La prevalencia promedio de la HTA en mayores de 60 años fue 48%, lo que representa un alto porcentaje de la población. Además, la prevalencia de la HTA se incrementó a medida que avanzaba la edad, en toda la población, siendo mayor en la costa sobre los 60 años de edad, en comparación con las otras regiones del país. Esto nos lleva a considerar que, la probabilidad de desarrollar hipertensión arterial es mayor en la costa que en la sierra y selva, a edades equivalentes, lo que podría estar en relación con el estrés, la alimentación, el modo de trabajo y el sedentarismo, es decir el modo de vida en las grandes ciudades, independientemente de la herencia y la genética.

La prevalencia de la hipertensión arterial es mayor en la costa (27,3%) que en la selva (22,7%) y la sierra (20,4%). El análisis de los resultados en la sierra demuestra que hay una mayor prevalencia en las ciudades situadas a mayor altura, sobre 3 000 msnm (22,1%), cuando se compara con las ciudades localizadas por debajo de los 3 000 msnm (18,8%).

Estos resultados de la altura contrasta con lo que se había establecido que, en la sierra la prevalencia de la hipertensión arterial era menor cuando la altura era mayor. Este concepto fue basado en los resultados de diferentes investigadores peruanos, destacando las investigaciones de Ruiz y col, realizadas en Milpo, un asiento minero a 4 100 msnm8,9, 18, 28, en el cual encontraron una menor prevalencia usando otra definición de HTA. Otros autores, como Lorena, en el Cusco (3 400 msnm) y en el Valle Sagrado de los Incas (2 700 msnm) señala una prevalencia de 10% y 3%, respectivamente, en 197913, y Mispireta, en Tarma (2 900 msnm), una prevalencia de 6%, en 198022.

Hay que señalar que estos estudios epidemiológicos fueron realizados en pequeñas poblaciones, algunos en asientos mineros, y con diferentes definiciones del HTA. En la actualidad, hay una serie de factores importantes en el aspecto socioeconómico, demográfico y epidemiológico en las tres regiones del país, que contribuyen a explicar estos cambios, tales como el incremento de la población en las ciudades por la migración del campo a la ciudad, lo que trae la urbanización, con cambios en el estilo de vida, como la alimentación, el sedentarismo y la industrialización, que conlleva el incremento del estrés. Se argumentó la posibilidad de la influencia racial para explicar esta menor prevalencia, ya que la población en las grandes alturas tiene un predominio de raza mestiza, con una minoría blanca y negra y de escasa raza amarilla.

En las ciudades de la selva, encontramos una prevalencia de 22,7%, lo que contrasta con resultados anteriores, que señalaban una prevalencia de 5%, debido a los mismos factores señalados anteriormente22.

La prevalencia de la HTA en las distintas ciudades del Perú no tiene un patrón de presentación y no existe una correlación entre el tamaño de la población, la altura de las ciudades, en relación con el nivel del mar y la selva. Así, el Callao, puerto principal en la costa del Perú, es la ciudad con mayor prevalencia (34,5%) y no es la ciudad más poblada. Por otro lado, Abancay, situada a 2 300 msnm, es la ciudad con menor prevalencia (12,4%); y, Cerro de Pasco, situada a mayor altura, tiene 17,7% de prevalencia. El análisis de los resultados de la HTA, cuando se aplica la definición del VII Comité Nacional Conjunto (2004), demuestra una mayor prevalencia de normotensos (presión ideal), en la sierra y selva, en comparación a la costa, que tiene un comportamiento opuesto a la prevalencia de la hipertensión estadio I y II, siendo mayor en la costa que en la sierra y selva.

En la sierra, las ciudades situadas sobre los 3 000 msnm tiene una mayor prevalencia que en las ciudades de la sierra situadas a menor altura, debajo de los 3 000 msnm, debido a los mismos cambios de modo de vida señalados anteriormente. La distribución de los hipertensos, en sistólicos, diastólicos y sistodiastólicos, demuestra que los hipertensos diastólicos aislados son los de más prevalencia en las tres regiones del Perú, siendo mayor en la sierra.

Se postuló la existencia de una relación 'directa-parcial' significativa entre hematocrito y presión arterial diastólica, especulando que la policitemia existente en los habitantes de la altura, que es el resultado de la hipoxia crónica, compensaría la disminución de la presión diastólica producida por vasodilatación e hipervascularización, incrementando el área de la sección transversal y disminuyendo la resistencia periférica al flujo, lo que llevaría a disminuir la presión arterial sistémica; ello da como resultado que las cifras de la presión arterial diastólica sean similares a las del nivel del mar. Esta compensación fisiológica explicaría por qué la presión arterial diastólica es mayor en habitantes de la sierra que viven a un nivel mayor de 3 000 msnm, donde este mecanismo compensatorio no estaría presente, debido a una mayor policitemia. Así mismo, este mecanismo compensatorio explicaría por qué la prevalencia de la hipertensión diastólica es más alta en los habitantes de mayor edad, que tienen una mayor rigidez de los vasos, a diferencia de los adultos jóvenes, donde la hipervascularidad sanguínea estaría compensada por una mayor elasticidad de las paredes arteriales, disminuyendo la resistencia periférica al flujo, que al final disminuye la presión arterial sistémica36.

Solo 44,9% de la población total de hipertensos tenía conocimiento de su condición de hipertensos. De estos hipertensos, 27,3% no recibía ningún tipo de tratamiento; y, de los 72,7% que recibía algún tratamiento, solo prácticamente la mitad de ellos (45,1%) estaba compensado con tratamiento médico y/o farmacológico.

En conclusión, del total de hipertensos solo 14,7% estaba adecuadamente controlado, porcentaje muy bajo y que debe ser tomado en cuenta por las instituciones de salud del Estado, en colaboración con las sociedades médicas, que deben realizar campañas de difusión a nivel nacional.

Los resultados del tratamiento farmacológico que recibían los hipertensos, muestran que la gran mayoría (82,2%) recibía inhibidores de la enzima convertidora (ECA), seguidos por los calcioantagonistas dihidropiridínicos (12%) y luego otros hipotensores, lo que podría estar en relación con el costo de la medicina.

Los datos epidemiológicos son obtenidos del Estudio sobre factores de riesgo cardiovascular por los doctores Luis Segura y Régulo Agusti, y en colaboración con múltiples investigadores nacionales y auspiciado por la Sociedad Peruana de Cardiología.

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CORRESPONDENCIA

Dr. Régulo Agusti C.

ragustic1@terrra.com.pe

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Epidemiología de la Hipertensión Arterial en el Perú

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Citado por SciELO Similares en SciELO SIMPOSIO: HIPERTENSIÓN ARTERIAL Epidemiología de la Hipertensión Arterial en el Perú Epidemiology of Arterial Hypertension in Peru 1 Médico Cardiólogo. Profesor Emérito, Universidad Peruana Cayetano Heredia. Ex Presidente de la Sociedad Peruana de Cardiología Objetivos: Determinar la prevalencia, conocimiento, tratamiento y control de la hipertensión arterial en el Perú.

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Prevalencia y factores de riesgo asociados con la hipertensión y la prehipertensión en una población trabajadora a gran altura en China: un estudio transversal

Año: 2017
Estudio transversal
- Este estudio indica que la prevalencia de hipertensión en la población estudiada fue del 28,1% y esta asociado a factores de riesgo como: edad, el sexo, la etnia, el puesto de trabajo, el sobrepeso u obesidad, el consumo frecuente de alcohol, los antecedentes familiares de hipertensión, diabetes e hiperuricemia.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5664790/

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Abstract

Background

Little information is available on the epidemiology of hypertension and prehypertension at high altitude in China, the aim of this study was to determine the prevalence of hypertension, prehypertension and their risk factors among Chinese working population at high altitude regions.

Methods

A cross-sectional survey was performed in an occupational sample of 4198 employees aged 20-59 years on Qinghai-Tibet Plateau between May to July 2013. Information from a self-administered questionnaire, physical examinations and laboratory measurements were obtained from each participant. Multivariable analysis was performed to determine the association of various risk factors with hypertension and prehypertension.

Results

The total crude prevalence of hypertension and prehypertension was 28.1 and 41.5%, respectively; the overall standardized prevalence of hypertension and prehypertension was 26.7 and 41.3%, respectively. Multivariate logistic regression showed that age, sex, ethnicity, job position, overweight or obesity, frequent drinking, family history of hypertension, diabetes and hyperuricemia were risk factors for hypertension, and age, sex, education, job position, overweight or obesity, current smoking and family history of hypertension were risk factors for prehypertension. Among the hypertensives, 36.5% were aware of their condition, 19.4% were being treated and 6.2% had their blood pressure (BP) controlled; among the treated hypertensives, 31.9% had their BP under control.

Conclusions

There is a high prevalence of hypertension and prehypertension in the working population at high altitude in China, but with very low awareness, treatment and control rates. Workplace-based BP screening and intervention programs that aim to modify risk factors such as high BMI, tobacco use, alcohol consumption and inappropriate use of antihypertensive medicine are urgently needed.

Electronic supplementary material

The online version of this article (doi:10.1186/s12199-017-0634-7) contains supplementary material, which is available to authorized users.

Keywords: Hypertension, Prehypertension, Risk factors, Workplaces, High altitude

Background

Cardiovascular disease (CVD) is the leading cause of death and disease burden globally, and hypertension (HTN), defined as systolic blood pressure (SBP) ≥140 mmHg and/or diastolic blood pressure (DBP) ≥90 mmHg, or taking antihypertensive medicine [ 1], is the most important preventable risk factor for CVD in China [ 2]. With the rapid economic development and urbanization of China, the prevalence of HTN has risen substantially. It is estimated that 325 million Chinese adults, 29.6% of the Chinese adult population, had HTN in 2010 [ 3]. However, this number does not include the prehypertension (PHT, representing a SBP of 120-139 mmHg and/or a DBP of 80-89 mmHg [ 1]), which is also identified as being independently associated with increased risk of HTN and CVD. Several national surveys reveal that PHT affects more than 20% of the general adult population, most commonly among middle-aged adults [ 4- 6].

Most epidemiological studies have focused on the prevalence of HTN, PHT and their related risk factors in general Chinese population. However, little attention has been devoted to the occupational population, especially those working at high altitude areas. High altitude was considered as an altitude greater than 2400 m above the sea level [ 7], and exposure to hypoxia environment at high altitude is increasingly being identified as a risk factor for HTN [ 8]. For instance, a recent systematic review has indicated a 2% increase in the prevalence of HTN among the Tibetans with every 100 m increase in altitude in Tibet [ 9]. From an international perspective, the working population has been identified as the high-risk group for CVD due to the clustering of CVD risk factors such as raised blood pressure (BP), high BMI, and smoking [ 10- 12]. There is a large number of workers on Qinghai-Tibet Plateau e.g., railroad construction, power maintenance, and their health status are closely related with the social stability and economic growth. Furthermore, the workplace is an ideal setting for health promotion as working population spend a considerable amount of their daily activity there [ 13]. Relevant information on the prevalence and determinants of HTN and PHT in the occupational samples at high altitude is crucial for establishing goals for effective workplace-based intervention programs.

The aim of the present study was to determine the prevalence of HTN and PHT and explore their potential risk factors in a convenience sample of young and middle-aged employees of 23 workplaces at China's high altitude areas.

Methods

Study design and participants

The study was conducted among employees of a state-owned grid corporation in the Qinghai Province of China. This corporation was a special large-sized enterprise operating the business of construction, rehabilitation, operation and maintenance of power grid, and it was composed of 23 geographically separate subsidiaries located in Qinghai Province, which were the workplaces investigated in this study. Qinghai lies in western China - on the northeastern part of the Qinghai-Tibet Plateau with an average altitude above 3000 m, and the altitudes of the workplaces in our study follow a scale of 2600 to 3700 m. The corporation comprised approximately 6000 full-time employees at the time of survey, and the general manager of this corporation agreed to implement the investigation during the working hours and salary was not deducted for leaving work to participate in the survey. In total, 4975 employees who had been working at the corporation for at least 2 years were examined, and among them 777 employees were excluded from the study for failing to complete either a questionnaire survey, a mandatory physical examination, or a laboratory measurement. Therefore, 4198 employees aged 20-59 years were finally included, representing a convenience sample.

Data collection

The data collection period was between May to July 2013. All subjects were asked to complete a self-administered, structured questionnaire in the meeting rooms of their workplaces. Clerical errors and blanks were checked by trained research staff and then corrected by subjects on-site. The questionnaire was divided into three main sections to obtain data on subjects' demographic characteristics, health behaviors, and HTN-related information.

To be specific, in Section A (demographic characteristics), subjects' age, sex, ethnicity (Han, Tibetan, or others), educational level (primary, middle, high school, college, or university and above) and job position (supervisor, or general staff) were asked. In Section B (health behaviors), subjects were asked "Do you currently smoke cigarettes?" (yes, one or more per day/yes, less than one cigarette per day/no, I quit smoking/I have never smoked) and "How often did you drink in the past month?" (daily/frequently (3 to 6 days a week)/occasionally (1 to 2 days a week)/did not drink any). In section C (HTN-related information) subjects were asked "Do any of your immediate family members (including parents, grandparents, and siblings) have HTN?" (yes/no), "Have you ever been told by a doctor or other healthcare professional that you had HTN?" (yes/no), and for those with HTN, they were also asked "Because of your HTN, are you now taking prescribed medicine?" (yes/no).

Measurements of BP, height and weight, and biochemical analysis of blood samples were all conducted in examination centers of designated hospitals. Subjects were suggested to avoid drinking, smoking, coffee, tea and exercise for at least 30 min prior to the measurement. BP measurements were taken after the subjects resting in a seated position quietly for at least 5 min. Throughout the survey, BP was measured three times at 5 min intervals in the morning. A previously validated electronic sphygmomanometer (Omron HEM-7201, Omron, Dalian, China) was used for the BP measurements in our study, this automated BP device has good accuracy and is recommended for use in adults at high altitudes [ 14]. The mean of the second and third readings defined a subject's BP. Body height and weight were measured and body mass index (BMI) was then calculated as weight (kg) divided by height squared (m ²). These indexes were all measured by trained physicians following standard protocols [ 15]. After an overnight fast of at least 8 h, the subjects' venous blood samples were obtained by trained physicians to test the levels of total cholesterol (TC), triglycerides (TG), serum uric acid (SUA) and fasting blood glucose (FBG) in the laboratory.

Definitions

Subjects were diagnosed with normotension (NTN), prehypertension (PHT) and hypertension (HTN) by trained physicians, according to the criteria from the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC-7) [ 1]. HTN was defined as SBP ≥140 mm Hg and/or DBP ≥90 mm Hg, or current treatment with antihypertensive medications. PHT was defined as a SBP between 120 and 139 mm Hg and/or a DBP between 80 and 89 mm Hg. NTN was defined as SBP < 120 mm Hg and DBP < 80 mm Hg. BP Control was defined as an average SBP and DBP lower than 140/90mmHg while on treatment. Diabetes was defined as a FBG ≥7.0 mmol/L or a self-reported previous diagnosis of diabetes by the doctors. Based on the criteria of the 2007 Chinese Guidelines on Prevention and Treatment of Dyslipidemia in Adults [ 16], high TC was defined as total cholesterol ≥6.22 mmol/L and high TG as triglyceride ≥2.26 mmol/L. Subjects with BMI 24.0-27.9 kg/m ² was defined as overweight and BMI ≥28.0 kg/m ² as obesity, and overweight or obesity referred to a BMI ≥24.0 kg/m ² [ 17]. Criteria for hyperuricemia were SUA levels ≥357 μmol/L in women and 416 μmol/L in men, respectively [ 18]. Current smoking was defined as subjects who reported smoking either every day or some days at the time of survey. Frequent drinking was defined as subjects who reported drinking daily or frequently during the past 30 days preceding the survey.

Statistical analysis

All continuous variables are presented as mean (SD), except for TC and TG, which are described by median (interquartile range) because of the skewed distribution. Categorical variables are presented as numbers (percentages). Prevalence rates in the overall population were calculated by the direct standardized method, according to the Sixth National Population Census of China (2010) [ 19]. One-way ANOVA was used to compare continuous variables with normal distribution among inter-group, and Student-Newman-Keuls (SNK) test was used for pairwise comparisons. Kruskal-Wallis test was used to compare continuous variables with non-normal distribution among inter-group and Wilcoxon rank-sum test was used for pairwise comparisons. Categorical variables were analyzed by Chi-squared test and Bonferroni adjustment was applied for pairwise comparisons in which a Bonferroni-adjusted p-value <0.05/3 or 0.017 was considered to be statistically significant. Multivariable logistic regression analyses were used to explore the risk factors of HTN (vs NTN) and PHT (vs NTN), with HTN and PHT serving as the dichotomous outcome variables, and sex, age, ethnicity, education, job position, overweight or obesity, current smoking, frequent drinking, family history of HTN, diabetes, hyperuricemia, high TC and high TG, as the candidates for inclusion in the analyses. All data analyses were conducted using SAS 9.4 (SAS institute, Cary, NC, USA) and a two-sided p- value <0.05 was considered statistically significant.

Results

Prevalence of HTN and PHT

Of the 4198 subjects, 3026 (72.1%) were men and 1172 (27.9%) were women, and the sex ratio (men: women) was 2.58:1. The mean (SD) age of the total was 39.77 (8.92) years, 39.75 (9.37) years for men and 39.82(7.62) years for women, respectively. Han Chinese were overrepresented and accounted for 90.4% of the total. Among all the subjects, 3545 (84.4%) were inhabitants and 653 (15.6%) were migrants from inland China, and the corresponding figures for Han Chinese were 3176 (83.7%) and 618 (16.3%), respectively. Overall, there were 1180 (28.1%) with HTN, 1744 (41.5%) with PHT, and 1274 (30.4%) with NTN. Age- and sex-standardized prevalence rates of HTN and PHT among subjects were 26.7% and 41.3%, respectively. The age-standardized prevalence of HTN and PHT was both higher in men than in women (30.8% vs 16.4%, 43.5% vs 36.1%, respectively).

Figure depicts the age-specific crude prevalence of HTN and PHT in men, women, and all subjects. Men had significantly higher prevalence of HTN and PHT compared with women (32.3% vs 17.3 and 43.8% vs 35.8%, respectively; p <0.001). The age-specific prevalence of HTN (Fig. ) increased distinctly with age in both men and women ( p <0.001). In men, the prevalence age-specific of PHT (Fig. ) increased up to the age of 30 then decreased with age ( p <0.001), whereas the opposite trend was observed in women participants ( p <0.05). For each age group up to 50, men had a higher age-specific prevalence of PHT (Fig. ) than that of women, while the reverse pattern was observed in those older than 50 years, with women having greater age-specific prevalence of PHT.

Characteristics of subjects according to BP status

Characteristics of subjects according to BP status is presented in Table . Men, Han ethnicity, those with high school education or less, supervisors, overweight or obese individuals, current smokers, frequent drinkers, diabetics and hyperuricemic increased significantly from NTN to PHT, and then eventually to HTN. There was an exception of this trend in the cases of individuals with high TG, higher degree, and those who had a family history of HTN. Moreover, there were significant positive relationships of age and anthropometric indices (BP, BMI, TC, TG, FBG, SUA), but inverse associations of medium education (those with diplomas or basic degrees) and general staffs with PHT and HTN.

Table 1

The prevalence rates of overweight or obesity, high TC, high TG, current smoking, frequent drinking, family history of HTN, diabetes and hyperuricemia among subjects were 39.1% (men: 45.7% vs women: 22.1%; p <0.001), 2.9% (men: 3.3% vs women: 1.7%; p <0.01), 18.7% (men: 22.5% vs women: 8.9%; p <0.001), 43.5% (men: 59.2% vs women: 3.2%; p <0.001), 10.2% (men: 13.8% vs women: 0.9%; p <0.001), 37.2% (men: 34.4% vs women: 44.5%; p <0.001), 5.4% (men: 6.7% vs women: 2.1%; p <0.001) and 26.1% (men: 29.6% vs women: 17.0%; p <0.001), respectively. [see Additional file 1].

Risk factors associated with HTN and PHT

Table shows the various risk factors associated with HTN and PHT by the multivariable logistic regression analysis. Men, higher age and job position, overweight or obesity, and family history of HTN were significantly associated with HTN and PHT. Han ethnicity, frequent drinking, diabetes and hyperuricemia were risk factors for HTN but were not for PHT. Compared to subjects with a high school or less level of education, those with a higher degree were less likely to have PHT. Current smoking was not significantly associated with HTN but was found to be negatively associated with PHT.

Table 2

Awareness, treatment and control of hypertension by sex

As shown in Table , among the 1180 hypertensive individuals, 430 were aware of their condition. The awareness of HTN was 36.5% and there was significant difference between men and women ( p <0.001). The treatment of HTN was 19.4%, only 229 individuals with HTN reported that they were taking antihypertensive drugs to treat HTN, of which 73 (31.9%) had their BP under control, resulting in a rate of HTN control at 6.2%.

Table 3

Discussion

Our findings showed that the adjusted prevalence of HTN was 26.7%, which is comparable with some studies among Chinese adults in other regions [ 2, 20], ranging from 24.6 to 41.0%. In a nationally representative sample of 15 019 working-age Chinese adults, the prevalence of HTN was 23.5% [ 21], which is lower than the corresponding figure in this study. Similarly, the present observation was higher than the HTN prevalence in Ireland (12.8%) [ 11] and Hungary (22.6%) [ 10], while lower than that in America (29.5%) [ 5]. Equally important was the finding of 41.5% of subjects identified as PHT, and the adjusted prevalence of PHT was 41.3%, which is considerably higher than prior estimates for adults in China (21.9%) [ 4] and America (23.1%) [ 5]. Growing evidence suggests that individuals with PHT would have a significant higher proportion of developing to HTN and risk of CVD within a few years [ 10], compared to those with NTN. Considering the average age of this working population, 39.8 years, is younger than the general population, and they spend one-third of their daily activity at work. Hence, effective measures targeting at employees with PHT are urgently needed to be developed at the workplaces.

HTN and PHT, which affected more than two-thirds (69.9%) of the working population at high altitude in China, represents a major public health concern. The possible reasons for this high prevalence of HTN and PHT among young employees may be due to the high prevalence of overweight/obesity (39.1%) and smoking (43.5%), as well as the high proportion of family history of HTN (37.2%). Meanwhile, chronic exposure to high-altitude hypoxia environment may also lead to elevated BP [ 9].

In accordance with previous reports [ 10, 22], men had a higher overall prevalence rate of HTN and PHT than women, which resulted from the higher prevalence of metabolic risk factors for HTN and PHT [ 2, 22] (i.e., overweight or obesity, high TC, high TG, and diabetes) found in men. Our data showed that the prevalence of HTN increased with age in both men and women whereas the prevalence of PHT decreased in men older than 30 years. Moreover, there was an increase in the prevalence of PHT for women as age increased, with a peak in the prevalence of PHT for women between the ages of 50 to 59 years old, similar results are reported in adults from the United States [ 23]. It seems that the changing levels of hormones with age between sexes can interpret this difference [ 22].

In our survey, subjects with PHT had intermediate levels of BMI, TC, TG, rates of overweight or obesity, smoking, and drinking and these values increased significantly in parallel to BP. In the multivariable analysis, sex and age were significantly associated with HTN and PHT, which were confirmed in some studies [ 2, 22]. Overweight and obesity are important modifiable risk factors of HTN and PHT [ 2, 4, 24], as demonstrated in our study. When obesity coexists with elevated BP, it may further increase the development of CVD [ 24], thus, weight control should be prioritized for employees with high BP. Some studies have indicated that high TC and high TG are causes of HTN or PHT [ 2, 4, 22], and it was also noted that rising levels of TC and TG were related with HTN and PHT in our results. However, these two factors were not confirmed after adjusting for confounders. Our study showed that current smokers were at lower risk of PHT, an observation which was also described in other studies [ 25]. The reason for this association is still unclear and we will continue to study it. In earlier studies, alcohol use has been found to be a significant risk factor of both HTN and PHT [ 22, 24]. We observed that frequent drinking were predictors of HTN but not for PHT, this dichotomy was probably related with the different definitions for drinking.

An earlier study conducted in six provinces of China indicated that the prevalence of HTN varied widely among Chinese ethnic groups, and Han Chinese had higher prevalence of HTN [ 6]. Consistent with this trend, we found that Han Chinese had a higher risk of HTN compared with non-Han. The difference in demographic factors, lifestyle and population genetics structure of the studied population may underlie this variability [ 26]. Our study confirmed the findings from previous study in northeast China that high levels of education is associated with a lower risk of PHT [ 25]. Individuals with higher degree were supposed to have adequate HTN knowledge [ 27], thus they were better informed about BP management and developed healthy lifestyles subsequently. In addition, studies showed that employees belonging to higher job position had a higher risk of developing HTN and PHT [ 20, 25], similar conclusion was found in our study. The possible explanations are following: 1) Supervisors may suffer from higher psychosocial work stress than general staffs, and high work stress has been shown to be associated with increased BP [ 28]. 2) Compared with the general staffs, the supervisors usually spent more time sitting at desk and working on computers, and a decrease in physical activity may also cause the high BP.

We also analyze the relationship between family history of HTN and elevated BP. After adjusting the potential confounders, our results indicated that normotensive individuals with a family history of HTN tend to have greater risk of HTN and PHT than those without. Therefore, primary prevention strategies should be targeted at subjects with a family history. We observed that the levels of FBG and SUA, and proportion rates of diabetes and hyperuricemia increased with the elevated BP. Diabetes and hyperuricemia were independent predictors for HTN after adjusting sex, age and other risk factors, which correspond with prior studies [ 20, 24, 29]. This finding suggests the importance of early detection of FBG and SUA among those with elevated BP.

The rates of awareness, treatment and control of HTN in this study are lower than that previously reported in western China (36.5% vs 43.6%,19.4% vs 35.8%, 6.2% vs 9.3%) [ 21] and in other developed countries [ 30], although higher than that in the China Kadoorie Biobank Study [ 31]. Divergent results may partly be explained by characteristics of research including differences in region, age, occupation, etc. For instance, 87.8% of subjects in our survey were under 50 years old, working and living at less developed western China, the young population may never have measured their BP before or been told the dangers of rising BP. It is noteworthy that among those who underwent antihypertensive treatment, only about one-third achieved BP control, which was probably influenced by the medicine adherence of the hypertensive patients [ 15]. Moreover, the choice of antihypertensive drugs at high altitude regions can also have an impact on BP control [ 32].

It should be noted that this study has several limitations. First, the data came from a cross-sectional survey in a homogenous working group at high altitude, which would not be representative of the entire working population. Thus the generalizability of current reported information to other regions of China could be limited. Second, the design of cross-sectional study leaves open for interpretation of casual relationships between the development of HTN, PHT and their risk factors, which implies that our results must be interpreted with some caution. Third, the special local diet of Qinghai-Tibet plateau, including butter tea, beef and mutton, all of which containing high salts and cholesterols and may contribute to the elevation of BP [ 33], however, diet and salt intake was not included due to unavailable evidence-based data in our survey. Fourth, work stress might raise BP [ 28], while it was not investigated in this study. Finally, our results are lacking information on individual's working altitude, as well as the changes of physiologic parameters at different working altitudes, e.g., oxygen saturation, resting heart rate, and indices of red blood cell. Those parameters are well-known to be influenced by chronic exposure to high altitude as body's compensatory responses to hypoxia environment [ 34], which could be associated with BP levels. Future study is needed to examine the physiologic parameters and identify the underlying mechanisms regarding the impact of altitude on BP.

Conclusions

This study suggests a high prevalence of HTN and PHT in a working population aged 20-59 years at high altitude in China, which may be predictive of high incidence of future CVD events. Men, higher age and job position, overweight or obesity, and family history of HTN are predictors of both HTN and PHT. Despite the high prevalence of HTN, the rates of awareness, treatment and control were unacceptable low. To tackle the challenge, workplace-based BP screening and intervention programs that aim to modify risk factors such as high BMI, tobacco use, alcohol consumption and inappropriate use of antihypertensive medicine should be conducted.

Acknowledgements

Not applicable.

Funding

This research received no specific grant from any funding agency in the public, commercial or not-for-profit sectors.

Availability of data and materials

All data generated or analyzed during this study are included in this published article ( and its Additional file).

Authors' contributions

YW conceived and designed the study, YS analyzed the data and wrote the paper, CC reviewed and edited the paper, JZ helped prepare the database and helped in the data analysis, YJ collected the data and helped in the data quality assurance, BN edited the paper. All authors read and approved the final manuscript.

Competing interests

The authors declare that they have no competing interests.

Consent for publication

Not applicable.

Ethics approval and consent to participate

All subjects gave their informed consent for inclusion before they participated in the study. The study was conducted in line with the Declaration of Helsinki, and the protocol was approved by the ethics committee at Peking University (Reference number: IRB00001052-13023).

Publisher's Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Abbreviations

Additional file

Footnotes
Electronic supplementary material
The online version of this article (doi:10.1186/s12199-017-0634-7) contains supplementary material, which is available to authorized users.

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Prevalence and risk factors associated with hypertension and prehypertension in a working population at high altitude in China: a cross-sectional study

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Little information is available on the epidemiology of hypertension and prehypertension at high altitude in China, the aim of this study was to determine the prevalence of hypertension, prehypertension and their risk factors among Chinese working population at high altitude regions.

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La ingesta excesiva de energía y la obesidad son las principales causas de la hipertensión, la obesidad se asocia con una mayor actividad de los sistemas nervioso simpático y renina-angiotensina-aldosterona, posiblemente con otra actividad mineralcorticoide. Además, el alto consumo de cloruro de sodio predispone fuertemente a la hipertensión, aumento del consumo de alcohol puede elevar de forma aguda la presión arterial.

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Abstract

The incidence and severity of hypertension are affected by nutritional status and intake of many nutrients. Excessive energy intake and obesity are major causes of hypertension. Obesity is associated with increased activity of the renin-angiotensin-aldosterone and sympathetic nervous systems, possibly other mineralcorticoid activity, insulin resistance, salt-sensitive hypertension and excess salt intake, and reduced kidney function. High sodium chloride intake strongly predisposes to hypertension. Increased alcohol consumption may acutely elevate blood pressure. High intakes of potassium, polyunsaturated fatty acids, and protein, along with exercise and possibly vitamin D, may reduce blood pressure. Less-conclusive studies suggest that amino acids, tea, green coffee bean extract, dark chocolate, and foods high in nitrates may reduce blood pressure. Short-term studies indicate that specialized diets may prevent or ameliorate mild hypertension; most notable are the Dietary Approaches to Stop Hypertension (DASH) diet, which is high in fruits, vegetables, and low-fat dairy products, and the DASH low-sodium diet. Long-term compliance to these diets remains a major concern.

Autonomic nervous system activity changes in patients with hypertension and overweight: role and therapeutic implications.

Valensi P. Valensi P. Cardiovasc Diabetol. 2021 Aug 19;20(1):170. doi: 10.1186/s12933-021-01356-w. Cardiovasc Diabetol. 2021. PMID: 34412646 Free PMC article. Review.

Impact of Micronutrients on Hypertension: Evidence from Clinical Trials with a Special Focus on Meta-Analysis.

Chiu HF, Venkatakrishnan K, Golovinskaia O, Wang CK. Chiu HF, et al. Nutrients. 2021 Feb 10;13(2):588. doi: 10.3390/nu13020588. Nutrients. 2021. PMID: 33578935 Free PMC article. Review.

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national center for biotechnology information

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The effect of nutrition on blood pressure - PubMed

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The incidence and severity of hypertension are affected by nutritional status and intake of many nutrients. Excessive energy intake and obesity are major causes of hypertension. Obesity is associated with increased activity of the renin-angiotensin-aldosterone and sympathetic nervous systems, possib ...

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Factores asociados a la hipertensión arterial: una revisión sistemática
Año: 2020
Tipo de estudio: Revisión sistemática
Resultados: Los factores más encontrados relacionados con la mayor probabilidad de padecer hipertensión arterial fueron la edad y el Índice de Masa Corporal (IMC). Otros factores asociados a la enfermedad fueron: género (masculino), escolaridad (educación inferior), renta (renta inferior) y circunferencia de la cintura (alta). Nunca haber fumado, nunca haber consumido alcohol y el color blanco de la piel fueron características relacionadas con una menor probabilidad de padecer hipertensión arterial. Como se ha demostrado, demográfico, socioeconómico, las características conductuales y antropométricas son factores importantes asociados a una mayor probabilidad de padecer hipertensión arterial en la población adulta. Sin embargo, si bien la mayoría de los factores asociados con ella son susceptibles de intervención, se necesitarán políticas de promoción de la salud más amplias para reducir las desigualdades socioeconómicas en la prevalencia de la enfermedad.

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A hipertensão arterial sistêmica (HAS) é o maior fator de risco para mortalidade no mundo. Estima-se que em 2008, 12,8% dos óbitos foram decorrentes da HAS. A HAS contribuiu nas últimas décadas para o aumento da carga de cardiopatias, acidentes cerebrovasculares, insuficiência renal e para as incapacidades prematuras.

Segundo estimativas da Organização Mundial de Saúde (OMS), em 2014, 22,3% da população mundial com 18 anos ou mais sofria de HAS. Observam-se desigualdades entre os países do mundo, pois enquanto nos países de baixa renda a prevalência de pessoas acometidas pela HAS foi de 27,6%, nos países de alta renda foi de apenas 18,5%3 World Health Organization (WHO). Indicator and Measurement Registry [Internet] [acessado 2016 Jun 10]. Disponível em: http://apps.who.int/gho/indicatorregistry/App_Main/browse_indicators.aspx. Acesso em: 10 de junho de 2016 ³
http://apps.who.int/gho/indicatorregistr... .

Os estudos sobre Carga Global da Doença (GBD) apontam que a HAS aumentou substancialmente entre 1990 e 2015, assim como os óbitos e os anos de vidas perdidos por alguma incapacidade associada à HAS. O último GBD de 2015 destacou que todos os fatores de risco estudados, juntos, foram responsáveis por 57,8% (IC95% 56,6-58,8) dos óbitos e 41,2% dos anos de vida perdidos por incapacidade (DALY). A HAS foi o fator de risco que mais contribuiu para do DALY mundial, superando tabagismo e obesidade.

A prevalência de HAS sofre influência de múltiplos fatores, com destaque para os demográficos, hereditários, socioeconômicos, comportamentais e antropométricos. A maioria desses fatores podem ser controlado ou modificado, sendo então possível reduzir a incidência da hipertensão e de suas complicações. Assim, identificar os fatores associados, bem como conhecer a sua magnitude, constitui elemento de fundamental importância para subsidiar ações de controle da HAS.

Nesse sentido, o objetivo desse estudo foi identificar, por meio de revisão sistemática da literatura, os principais fatores epidemiológicos associados à HAS.

A revisão sistemática utilizou instrumento de coleta previamente formulado e registrado no PROSPERO5 National Institute for Health Research (NHS). University of York. PROSPERO: International prospective register of systematic reviews [Internet]. [acessado 2016 Jun 10]. Disponível em: http://www.crd.york.ac.uk/PROSPERO/ ⁵
http://www.crd.york.ac.uk/PROSPERO/... , base internacional de revisões sistemáticas em saúde e assistência social do Centre for Reviews and Dissemination da Universidade de York. O formulário para extração das informações continha os seguintes itens: a referência completa do artigo, o país de publicação, o período da busca, o desenho de estudo, o local (país/cidade) do estudo, as variáveis analisadas, o método estatístico, os resultados encontrados para a associação entre as variáveis analisadas e a prevalência de HAS e a avaliação da qualidade metodológica dos estudos selecionados.

Os critérios de elegibilidade dos estudos foram: estudos observacionais com objetivo de determinar a associação entre HAS e os fatores demográficos, socioeconômicos, antropométricos e de estilo de vida; estudos cujas associações foram estimadas por meio da utilização de modelos de regressão ajustados; e que utilizaram critérios de seleção da população de estudo adequada ao delineamento proposto (seccional, coorte ou caso-controle). Foram excluídos aqueles que não descreveram o método de análise estatística ou que não utilizaram modelos de regressão ajustados, assim como aqueles que lidaram com populações restritas como gestantes ou doentes crônicos.

Estabelecidos os critérios de inclusão e exclusão e após registro do formulário de extração dos dados procedeu-se à busca nas bases bibliográficas de acesso online Pubmed, Lilacs, Scopus e Web of Science (WOS). Foram selecionados os artigos publicados nos últimos 10 anos, em inglês, espanhol ou português.

Na estratégia de busca nas bases bibliográficas com vocabulário controlado, Pubmed ( MeSH terms) e Lilacs ( DeCS terms), utilizou-se a combinação dos termos " Hypertension/epidemiology" e " risk factor", excluindo-se uma série de descritores referentes a termos diversos daqueles definidos por critérios de pesquisa: " lung", " pulmonary", " intracranial", " ocular", " european continental ancestry group", " white coat syndrome", " cerebrum", " brain", " genes", " adolecent", " infant newborn", " fetus", " proteins", " pragnancy", e " newborn ".

Estratégias equivalentes foram utilizadas no processo de busca nas bases bibliográficas Web of Science e Scopus que não usam vocabulário controlado. As duplicidades foram identificadas e excluídas em todas as bases por meio do programa EndNote X 7.0.1.

As buscas eletrônicas foram realizadas por dois revisores independentes (1ª etapa de seleção). Posteriormente procedeu-se à avaliação da adequabilidade dos títulos ao objetivo do estudo (2ª etapa de seleção). Os resumos então foram lidos e avaliados (3ª etapa de seleção). Todos os artigos cujos resumos se adequaram aos critérios da pesquisa foram selecionados para leitura na íntegra (4ª etapa de seleção). Os resultados de todas as etapas da seleção foram comparados e as discordâncias solucionadas por consenso entre os dois revisores, ou por um terceiro revisor, quando necessário.

A avaliação da qualidade metodológica baseou-se em quatro critérios: seleção adequada das populações de estudo (S); descrição das perdas e sendo esta inferior a 20% (P); descrição de instrumento de aferição do desfecho (D); e apresentação das estimativas brutas e descrição do processo de seleção das variáveis no modelo ajustado (A). Estes critérios foram propostos por Esteves et al. com base na Newcastle-Ottawa Scale, para avaliação de estudos de coorte e nas diretrizes STROBE para estudos seccionais.

As variáveis associadas à hipertensão foram classificadas como variáveis demográficas, socioeconômicas, antropométricas e de estilo de vida, a fim de facilitar a análise e comparabilidade dos estudos.

Nesta revisão sistemática, a divulgação dos resultados foi feita com base as diretrizes propostas pela Preferred Reporting Items for Systematic Reviews (PRISMA) .

De acordo com a busca eletrônica foram encontradas 5.236 referências, das quais 62 foram excluídas por duplicidade. Após leitura do título excluíram-se 4.979 referências por não atenderem ao objetivo da revisão. Um total de 195 resumos foram avaliados quanto à adequação aos critérios pré-estabelecidos, sendo 130 eliminados. Procedeu-se então à leitura completa dos 65 artigos restantes, dos quais 23 foram excluídos pelas seguintes razões: não realizaram análises ajustadas (oito); não apresentaram seleção adequada da amostra (oito); estudos com populações restritas (cinco); artigo de revisão (um); não apresentou a descrição da metodologia (um). Ao final de todo o processo foram selecionados para inclusão nesta revisão 42 artigos⁻ ( Figura 1).

Todos os estudos foram realizados com base em amostra composta por indivíduos com 18 anos ou mais, no entanto, as faixas etárias estabelecidas em cada artigo foram muito variadas. Vinte faixas etárias foram identificadas.

O Quadro 1 apresenta as variáveis demográficas, socioeconômicas, antropométricas e de estilo de vida encontradas nos estudos, o tipo de variável (dicotômica, nominal ou ordinal) e sua associação ou não com o desfecho hipertensão (maior chance, menor chance ou não associação).

As variáveis demográficas associadas à hipertensão foram idade (dezenove artigos), sexo (dezessete artigos), raça ou cor (sete artigos) e área de residência (seis artigos). Em apenas um artigo a variável idade não foi analisada de forma ordinal. Em apenas dois artigos a idade não se mostrou associada,. Nos demais artigos em que a idade foi considerada, observa-se um aumento progressivo da chance de ter HAS nos indivíduos com idade a partir dos 40 anos,,,⁻,,,,,,,⁻,.

A variável estado civil foi considerada em sete artigos, sendo estudada de forma dicotômica em três,, e nominal em quatro,,,. Os resultados encontrados foram diversos, em três artigos, ser casado foi relacionado a menor chance de ter HAS em relação a pelo menos uma outra categoria de estudo,,, mas nos outros, a associação com o desfecho não foi observada,,,.

A renda foi analisada de forma ordinal em sete dos oito artigos que utilizaram a variável. Ter menor renda foi associado a maior chance de ter HAS em três estudos,,, menor chance em um e não associado ao desfecho em quatro,,,. Três estudos utilizaram a posse de plano de saúde como variável,,, mas nenhuma associação foi encontrada.

A ocupação foi analisada em dois artigos,. Ser trabalhador manual/agricultor ou desempregado mostrou maior chance de ter HAS nos dois estudos.

Variáveis referentes ao hábito alimentar foram incluídas em onze artigos, com grande variação entre as características culturais avaliadas. Levando em consideração os dados apresentados pelos autores, foram agrupadas as variações alimentares de maneira dicotômica entre alimentação adequada e inadequada. A alimentação inadequada apresentou maior chance de ter HAS em apenas dois artigos,, menor chance em dois, e não mostrou associação com o desfecho nos demais,,,,,,.

Idade e IMC elevados foram as variáveis mais frequentemente encontrados nos artigos selecionados na presente revisão. Ambos representaram associação em cerca de metade dos estudos analisados. Merecem destaque ainda, as variáveis sexo, escolaridade, renda e CC, onde as categorias "sexo masculino", "menor escolaridade", "menor renda" e "circunferência de cintura elevada" foram associadas à maior chance de ter HAS em pelo menos três artigos. Indivíduos nas categorias "cor branca", "nunca fumou" e "nunca consumiu álcool" apresentaram menor chance de ter HAS em pelo menos três artigos.

A idade elevada é um fator associado HAS já conhecido na literatura especializada. O envelhecimento traz modificações fisiológicas do aparelho circulatório, aumentado assim a chance de desenvolvimento da HAS. O aumento da prevalência de idosos no mundo é apontado pelos especialistas como o fator explicativo de maior destaque para o aumento da prevalência de HAS em todo o planeta,. Dos dezenove estudos nos quais foi considerada na análise, em dezessete apresentou associação direta entre idade elevada e HAS.

Maior chance de ter HAS entre os homens foi encontrada em alguns artigos. Segundo a OMS, em análise referente ao ano de 2008, os homens apresentaram maior prevalência de HAS em todas as regiões do mundo. No Brasil, estudos baseados em informações de diagnóstico médico autorreferido mostram que a prevalência de HAS em mulheres foi mais alta,. Resultado semelhante foi observado na Pesquisa Nacional de Saúde (PNS) de 2013, onde a prevalência autorreferida de HAS foi maior entre as mulheres. Contudo, cabe ressaltar que quando foram consideradas as aferições da pressão arterial, a HAS foi mais prevalente entre os homens. Este fato reforça o argumento de que a maior utilização dos serviços de saúde explicaria a maior prevalência de HAS autorreferida entre as mulheres.

Ter cor branca apresentou menor chance de ter HAS em quatro artigos analisados. Alguns estudos apontam que indivíduos não brancos apresentam maior chance de desenvolver hipertensão por características genéticas,. No entanto, não existe consenso sobre esse argumento. Ao analisar a relação entre raça/cor com HAS é preciso levar em consideração fatores do contexto histórico, econômico e político-social, uma vez que pessoas de cor negra têm, em geral, maior vulnerabilidade social.

Entre as variáveis socioeconômicas mais encontradas destacaram-se a escolaridade e a renda. Quanto menor a escolaridade e a renda, maior a chance de ter HAS. Estudos apontam que tanto características socioeconômicas do nível individual quanto macroeconômicas estão associadas à maior chance de ter HAS em pessoas e populações de menor status socioeconômico. Destacam que indivíduos expostos às condições de fragilidade social e econômica, individuais ou das áreas nas quais residem, têm maior chance de desenvolver HAS,. No entanto, discutem que os mecanismos subjacentes a esta associação ainda precisam ser melhor explorados.

A obesidade apareceu como o principal fator antropométrico associado a HAS incluído nos artigos selecionados. De fato, a obesidade é um forte preditor das doenças cardiovasculares. Esse resultado torna-se ainda mais preocupante quando consideramos que o Brasil é o quinto país com maior prevalência de obesos, com 21% de obesos na população com mais de 18 anos em 2013.

Assim como a obesidade, a falta de atividade física regular aumenta a chance de doenças cardiovasculares e sua relação com maior prevalência de HAS é conhecida na literatura. Nesta revisão, ser fisicamente inativo representou maior chance de ter HAS em quatro artigos.

O tabagismo e o consumo de álcool são fatores de risco para doenças cardiovasculares conhecidos na literatura. Os efeitos do tabaco e álcool no sistema circulatório são nocivos aumentando o risco de HAS,. Os avanços dos estudos epidemiológicos mostraram que embora a baixa ingestão de bebidas alcoólicas leves possa ser benéfica à saúde, o consumo abusivo de álcool está diretamente associado à maior mortalidade cardiovascular.

O tabagismo aumenta a pressão arterial, dobra o risco de desenvolvimento da HAS e provoca uma maior variabilidade nos níveis pressóricos, podendo causar lesões nos órgãos-alvo. Além disso, um estudo sobre carga global da doença apontou que o tabagismo é responsável por 45% e 25% dos óbitos por infarto agudo do miocárdio e por doenças cerebrovasculares, respectivamente.

O método de definição da HAS variou entre aferições realizadas pelos estudos e autodeclaração de diagnóstico prévio. Grande parte dos que usaram aferição eram estudos internacionais, no Brasil, cinco estudos utilizaram a aferição da pressão arterial para definir os indivíduos hipertensos. O uso da aferição é um método mais robusto, uma vez que não está influenciado por fatores como acesso a serviços de saúde e memória do participante da pesquisa. Contudo, pelo menos desde a década de 1990, estudos conduzidos em diversos mostram que a hipertensão arterial autorreferida tem alta sensibilidade, especificidade e bons valores preditivos (positivos e negativos).

O presente estudo apresenta algumas limitações, a primeira diz respeito a estratégia de busca. Embora tenha sido feita de forma a abarcar o maior número possível de publicações, pode-se ter deixado de captar trabalhos relevantes por falhas na estratégia de busca por palavras chaves ou descritores. Outra limitação encontrada foi a impossibilidade de realizar a síntese dos resultados por meio de meta-análise, uma vez que a heterogeneidade demográfica, regional e cultural dos estudos reduziu sua comparabilidade.

Os fatores associados à HAS são multidimensionais e seu debate em todo o mundo ainda precisa de aprofundamento. Embora haja consenso entre os estudos acerca dos limites pressóricos para considerar um indivíduo hipertenso, o que garante comparabilidade, não há consenso entre os estudos sobre a seleção e categorização dos fatores associados à HAS. Além disso, há grande variação entre os efeitos desses fatores e sobre quais se mostraram associados à HAS.

Espera-se que os resultados desse trabalho contribuam para o debate sobre os fatores associados à HAS. O rápido processo de envelhecimento alerta para necessidade de programas voltados para o controle da HAS, especialmente entre indivíduos com 40 anos ou mais, cuja chance de desenvolver HAS nesse estudo mostraram-se crescente com a idade. A promoção de hábitos de vida saudáveis, como por exemplo prática de atividade regular e controle do peso corporal, aparecem como ações estratégicas para o combate da obesidade que apresenta tendência crescente e está altamente associada a HAS.

Outro aspecto importante foi renda e grau de escolaridade baixos destacados por esta revisão, indicando que esforços para a ampliação das políticas de promoção da saúde nas classes em desvantagem social são necessários para a redução das desigualdades socioeconômicas relacionadas à ocorrência de hipertensão. Tendo em vista que a HAS é um agravo silencioso e, portanto, diagnosticado e tratado com mais frequência entre aqueles com maior acesso à assistência de saúde, a diminuição dos fatores associados nos grupos de baixo nível socioeconômico contribuiria não apenas para a diminuição da incidência de HAS na população, mas também para a diminuição de cardiopatias, acidentes cerebrovasculares, e outras doenças relacionadas à hipertensão.

Destaca-se, assim, nessa revisão a importância de considerar os fatores passíveis de intervenção, e enfatizar a necessidade de políticas de promoção à saúde mais amplas para reduzir as desigualdades socioeconômicas e a da incidência de hipertensão. Consequentemente, acarretaria a redução das doenças associadas à hipertensão e das limitações e incapacidades, implicando, por sua vez, no aumento da esperança de vida saudável nas classes em desvantagem social.

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Fatores associados à hipertensão arterial: uma revisão sistemática

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A hipertensão arterial sistêmica (HAS) é o maior fator de risco para mortalidade no mundo. Estima-se que em 2008, 12,8% dos óbitos foram decorrentes da HAS. A HAS contribuiu nas últimas décadas para o aumento da carga de cardiopatias, acidentes cerebrovasculares, insuficiência renal e para as incapacidades prematuras.

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A nivel mundial, se estima que el 26 % de la población mundial (972 millones de personas) tiene hipertensión, y se espera que la prevalencia aumente al 29 % para el 2025. Siendo considerada como el principal contribuyente de enfermedades cardiacas y accidentes cerebrovasculares. En Perú, según la Encuesta Demográfica y de Salud Familiar 2017 (ENDES 2017), la prevalencia de hipertensión arterial es de 13,6%, con acentuadas diferencias entre varones (16,6%) y mujeres (10,7%). https://www.scielo.cl/scielo.php?script=sci_arttext&pid=S0034-98872019000500545&lng=en&nrm=iso&tlng=en

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Globally, an estimated 26% of the world's population (972 million people) has hypertension, and the prevalence is expected to increase to 29% by 2025, driven largely by increases in economically developing nations.The high prevalence of hypertension exacts a tremendous public health burden. As a primary contributor to heart disease and stroke, the first and third leading causes of death worldwide, respectively, high blood pressure was the top modifiable risk factor for disability adjusted life-years lost worldwide in 2013.

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What is the global prevalence of hypertension (high blood pressure)?

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Globally, an estimated 26% of the world's population (972 million people) has hypertension, and the prevalence is expected to increase to 29% by 2025, driven largely by increases in economically developing nations.The high prevalence of hypertension exacts a tremendous public health burden.