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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:681.)
© 2006 American Heart Association, Inc.

Editorials

Cholesteryl Ester Transfer Protein Inhibition

Effect on Reverse Cholesterol Transport?

Patrick C.N. Rensen; Louis M. Havekes

From the Departments of General Internal Medicine, Endocrinology, and Metabolic Diseases (P.C.N.R., L.M.H.) and Cardiology (L.M.H.), Leiden University Medical Center, and TNO-Quality of Life, Department of Biomedical Research (L.M.H.), Gaubius Laboratory, Leiden, The Netherlands.

Correspondence to Patrick C.N. Rensen, PhD, Leiden University Medical Center, Department of Endocrinology and Metabolic Diseases, C4-R81, Albinusdreef 2, P.O. Box 9600, 2300 RC Leiden, The Netherlands. E-mail P.C.N.Rensen@lumc.nl

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Statins, inhibitors of the key enzyme in the biosynthesis of cholesterol (ie, 3-hydroxy-3-methylglutaryl [HMG]-coenzyme A [CoA] reductase), are widely used as the prevailing strategy to combat atherosclerosis through reducing LDL cholesterol levels. Large-scale clinical trials have shown that statins markedly reduce coronary events.^1,2 A meta-analysis of 22 studies enrolling nearly 70 000 individuals indicated that an effective decrease of LDL cholesterol by 20% to 40% reduces non-fatal myocardial infarction or coronary heart disease mortality by 25%.³ Although of clear clinical benefit, lowering LDL cholesterol alone using statin monotherapy thus does not prevent 75% of all cardiovascular events, which has led to a considerable interest in targeting other lipid-related risk factors.

See page 884

Prospective epidemiological studies have shown a strong inverse correlation between HDL cholesterol levels and cardiovascular disease.⁴ In fact, a low HDL level, often seen in combination with elevated triglyceride (TG) levels, is the primary lipid abnormality in &50% of men with coronary heart disease.⁵ Recent studies revealed that high HDL cholesterol levels are indeed protective against plaque progression.⁶ It has been shown that pharmacological intervention leading to an increase of HDL cholesterol by 1% is associated with a 2% to 3% decrease in cardiovascular risk.⁷ Although the exact mechanisms through which HDL protects are unclear, HDL has been shown to have antioxidant, antithrombotic, and antiinflammatory properties,⁸ and to mediate the flux of excess cholesterol from peripheral cells to the liver followed by excretion via the feces in a process referred to as reverse cholesterol transport (RCT).⁹

Based . . . [Full Text of this Article]

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