Cholesterol is packaged into lipoprotein particles in the liver and intestine and transported to peripheral tissues for normal cellular function. Reverse cholesterol transport is the mechanism by which excess cholesterol is transported back to the liver and is facilitated by high-density lipoproteins (HDLs). Increased plasma concentrations of cholesterol within the low-density lipoprotein (LDL) contribute to atherosclerotic vascular disease that commonly affects the coronary, cerebral and peripheral vascular circulation. Incontrovertible evidence now supports the use of the ‘statin’ class of drugs to decrease vascular disease. Statins inhibit hepatic cholesterol synthesis, increase hepatic low-density lipoprotein cholestrol (LDLc) receptor expression and consequently decrease plasma LDLc, to reduce risk of myocardial infarction in people at widely varying risk of heart disease. At present, there is limited evidence to support the use of drugs that modify high-density lipoprotein cholesterol (HDLc) to reduce risk of heart disease
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