Abstract
It has been established that the level of plasma high-density lipoprotein (HDL)-cholesterol is inversely proportional to the risk of coronary heart disease (CHD). HDL particles are highly heterogeneous, particularly in terms of their biological activities, many of which are atheroprotective. For example, in addition to carrying out reverse cholesterol transport, HDL protects the vascular endothelium by inhibiting monocyte adhesion and the oxidative modification of low-density lipoprotein (LDL), eliminates some of the atherogenic products of LDL oxidation, and possesses antithrombotic activity, due to the inhibition of platelet activation and aggregation. Statin therapy has been shown to increase the level of plasma HDL-cholesterol. However, the clinical benefit of statin-induced elevation of HDL-cholesterol is unclear from trial data, perhaps as a result of the concomitant overwhelming risk benefit of statin-induced reduction of LDL-cholesterol.

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