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HDL Cholesterol and Protective Factors in Atherosclerosis Gerd Assmann and Antonio M. Gotto, Jr Circulation 2004;109;III-8-III-14 DOI: 10.1161/01.CIR.0000131512.50667.46
Circulation is published by the American Heart Association. 7272 Greenville Avenue, Dallas, TX 72514 Copyright © 2004 American Heart Association. All rights reserved. Print ISSN: 0009-7322. Online ISSN: 1524-4539

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HDL Cholesterol and Protective Factors in Atherosclerosis
Gerd Assmann, MD; Antonio M. Gotto, Jr, MD, DPhil
Abstract—Alow level of high-density lipoprotein cholesterol (HDL-C) is an important risk factor for cardiovascular disease. Epidemiological and clinical studies provide evidence that HDL-C levels are linked to rates of coronary events. The cardioprotective effects of HDL-C have been attributed to its role in reverse cholesterol transport, its effects on endothelial cells, and its antioxidant activity.Although some clinical trials suggest a benefit of raising HDL-C to reduce risk, further studies are needed, and HDL-C is still not considered a primary target of therapy in the National Cholesterol Education Program guidelines. However, HDL-C should be considered as part of the patient’s overall profile of established risk factors in determining treatment strategies. (Circulation. 2004;109[supplIII]:III-8 –III-14.) Key Words: atherosclerosis cardiovascular diseases cholesterol lipoproteins risk factors high-density lipoprotein (HDL)

he association between low levels of high-density lipoprotein cholesterol (HDL-C) and an increased risk for cardiovascular disease has been well established through epidemiological and clinical studies.1 This relationship is supported by the potentialantiatherogenic properties of HDL, including its mediation of reverse cholesterol transport, in which cholesterol from peripheral tissues is returned to the liver for excretion in the bile.2 This review considers the potential mechanisms by which HDL-C may exert its antiatherogenic effects, discusses disorders of HDL and how to interpret them in the clinical setting, and presents current and potentialtreatment strategies for patients with low HDL-C.

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particles. These lipid-poor particles are increased in extravascular compartments where reverse cholesterol transport takes place. 3 The origin of HDL particles with pre– electrophoretic mobility is not entirely clear. Several mechanisms have been proposed, including direct secretion into plasma from hepatocytes or enterocytes; release duringthe interconversion of various HDL subpopulations by phospholipid transfer protein (PLTP), cholesteryl ester transfer protein (CETP), or hepatic lipase (HL); or direct interaction of free apolipoproteins with cell membrane.4 HDL and Reverse Cholesterol Transport Mechanisms. Reverse cholesterol transport describes the transfer of cholesterol from nonhepatic cells to the liver.3,4 Lipid-free apo A-Ior lipid-poor pre– -HDL particles produced in the intestine or liver or shed during lipolysis of triglyceride-rich lipoproteins (TGRL) initiate efflux of phospholipids and cholesterol from cell membranes in a process facilitated by PLTP. Cholesterol in these nascent discoidal HDL particles is then esterified by lecithin-cholesterol acyltransferase (LCAT). Cholesteryl esters readily move to the...