Calcific aortic stenosis may be caused by progressive calcification of a congenitally bicuspid valve, when it typically presents in the fourth and fifth decades of life, or senile calcification of a morphologically normal tricuspid valve when it tends to present later in life (fig 1​1).). The disease appears to be an active process that has much in common with atherosclerosis and is probably mediated by mechanical stress (“wear and tear”), lipid deposition, and inflammation; significant coronary artery disease is present in approximately 50% of patients with calcific aortic stenosis and the two conditions share many of the same risk factors, with a similar level of risk (table 1​1).^1,2 Rheumatic disease of the aortic valve usually causes mixed stenotic and regurgitant lesions and is commonly associated with mitral valve disease.
Acquired aortic stenosis develops slowly and the cardiac output is initially maintained at the cost of a steadily increasing gradient across the aortic valve. The left ventricle becomes increasingly hypertrophied and coronary blood flow may become inadequate; patients may therefore develop angina, even in the absence of concomitant coronary disease. The fixed outflow obstruction limits the increase in cardiac output required on exercise and effort related hypotension and syncope may occur. Eventually the left ventricle can no longer overcome the outflow tract obstruction and left ventricular failure supervenes. Patients with aortic stenosis typically remain asymptomatic for many years but deteriorate rapidly when symptoms develop; thus, death usually ensues within 3–5 years of the onset of symptoms.