doi: 10.1161/01.CIR.0000035280.64322.31
(Circulation. 2002;106:2137.)
© 2002 American Heart Association, Inc.
Mini-Review: From Bench to Bedside |
New Perspectives on Atherogenesis
Role of Abnormal Triglyceride-Rich Lipoprotein Metabolism
From the Columbia University College of Physicians and Surgeons, New York, NY.
Correspondence to Henry N. Ginsberg, MD, Department of Medicine, PH 10-305, Columbia University, 630 West 168th St, New York, NY 10032. E-mail hng1@columbia.edu
Key Words: apolipoproteins • lipids • lipoproteins • atherosclerosis • hyperlipoproteinemia
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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Atherosclerosis, along with the resultant coronary artery disease (CAD), is a leading cause of mortality in industrialized countries. Significant attention has focused on the role of low-density lipoprotein (LDL) in the pathogenesis of CAD. A dyslipidemia characterized by a combination of abnormalities in the plasma levels of triglycerides and high-density lipoprotein (HDL) cholesterol, with or without elevated LDL cholesterol levels, affects many persons with premature CAD, however. In particular, both qualitative and quantitative abnormalities in circulating triglyceride-rich lipoproteins (TRLPs) may be a key factor in the development of CAD.1
A number of advances have led to an increased appreciation of TRLP concentrations as independent predictors of risk for CAD. First, the meta-analysis by Hokanson and Austin2 demonstrated that increases in plasma triglyceride levels were associated with increased risk for CAD events, even after adjusting for numerous other predictive factors. The meta-analysis was supported by a more recent prospective study by Jeppesen et al,3 which demonstrated that triglyceride levels were independent predictors of ischemic heart disease in men. Second, a number of studies have demonstrated that TRLPs, whether assembled in and secreted from the intestine or the liver, can penetrate the artery wall and initiate or aggravate atherogenesis. Third, during the last decade, we have gained a much more detailed understanding of the metabolic relationship between high levels of TRLPs, low levels of high-density lipoprotein (HDL) cholesterol, and an abnormally small, cholesterol-depleted, dense LDL.4 This review will attempt to bring together information from recent cellular, biochemical, physiological, and molecular studies to
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