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Omega 3 fatty acids

Limit production of VLDL in liver

Increase VLDL clearance by taking it back into the liver from the bloodstream

Reduce risk of myocardial infraction & stroke in patients

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•Coronary artery disease

•Carotid artery disease

•Peripheral artery disease

•Aneurysms

•Chronic kidney disease

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Fibrates

Reduce VLDL (decrease production & increase clearance)

PPARa nuclear receptor --> increase gene transcription for:

lipoprotein lipase → decrease VLDL

apoA1 and apoA2 → increase HDL level

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Raised lipoprotein(a)

Reduced high-density lipoprotein cholesterol (HDL-C)

Hypertension

Diabetes mellitus

Cigarette smoking

Obesity

Physical inactivity

Raised coagulation factors (e.g. factor VII, fibrinogen)

Raised homocysteine

Chronic hyperlipidaemia

Raised low-density lipoprotein cholesterol

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Plaques cause stenosis and limit blood flow

Leading to tissue ischemia

When the fibrous cap of a plaque ruptures, blood coagulation components come into contact with the thrombogenic plaque and produce thrombi.

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Cholesterol absorption inhibitors

Mainly reduce LDL and total cholesterol

Jejunum; acts by blocking transport protein --> cholesterol will not be absorbed

Use with diet and statins

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Inside growing atheroma, smooth muscle cells are transferred from the tunica media into the tunica intima. The smooth muscle cells and macrophages die in advanced lesions by apoptosis.

These dead cells derive the extracellular lipid that builds up the plaque composed of the necrotic lipid core

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Inside the intima, monocytes mature and transform into macrophages that uptake the oxidized LDL particles to yield foam cells.

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Endothelial cells express adhesion molecules capture monocytes (leukocytes) on their surfaces.

Adhesion of blood monocytes to activated endothelial cells leads to their migration into intima.

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Caused by various agents (hemodynamic and chemical stressors)

Results --> impairment of permeability barrier function, secretion of inflammatory cytokines, stimulation of adhesion molecules on the cell surface --> leukocyte recruitment, and altered antithrombotic properties and release of vasoactive molecules

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Process of forming plaques in the intima layer of arteries

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Accumulation of lipids in the intima of the arteries, narrowing the lumen and compressing the muscular layer

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Statins

Blocking of HMG-coA reductase inhibits the production pathway of cholesterol leading to a decrease in cholesterol level

Inhibit cholesterol synthesis: 1) stimulates the synthesis of LDL receptors  2) increase LDL-C uptake 3) decrease secretion of VLDL

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Complex particles that have central hydrophobic core of non-polar lipids, primarily triglycerides and cholesterol esters

Surrounded by hydrophilic membrane consisting of phospholipids, free cholesterol and *apolipoproteins

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Bile acid sequestrants

Liver uses cholesterol and other chemicals to produce bile acids → BAS binds to bile acids and remove from system → Bile acid level decreases, liver need to take cholesterol from bloodstream to make more bile acids

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Hardening and narrowing of the arteries caused by gradual fibrofatty plaques or atheroma within artery wall