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High-density lipoprotein cholesterol as a major risk factor for coronary artery disease

Dyslipidemia is a central factor in the development of coronary artery disease (CAD). The correction of elevated low-density lipoprotein cholesterol (LDL-C) plasma levels has traditionally been regarded as the principal goal of therapy in hypercholesterolemia. However, low levels of high-density lipoprotein cholesterol (HDL-C) also contribute significantly to the risk of cardiovascular disease. Over 50 years ago, it was observed that CAD patients had lower plasma HDL-C levels compared with healthy men.1 A landmark study by Miller and Miller in 19752 and important epidemiological studies such as the Framingham Heart Study suggested an association between HDL-C and CAD.3 For many years, however, these findings were considered to be of lesser relevance than observations linking LDL-C and atherogenesis.

HDL-C and atherogenesis

HDL-C is produced in the liver and small intestine. It is composed of hundreds to thousands of triglycerides and cholesteryl ester particles that are covered by a surface monolayer of phospholipids, a small quantity of free cholesterol, and one or more apolipoproteins. HDL-C is involved in reverse cholesterol transport transferring cholesterol from extrahepatic tissues to the liver for metabolism. This transport mechanism may contribute to the antiatherogenic properties of HDL-C by aiding the efflux of cholesterol from the artery wall. In addition, reverse cholesterol transport may also reduce macrophage activation and contribute to the lesion-stabilizing actions of HDL-C. HDL-C may also beneficially affect atherogenesis by transporting natural antioxidants. Apolipoprotein A-I, the major protein component of high-density lipoprotein, and 2 enzymes, paraoxonase and platelet-activating factor acetylhydrolase, appear to diminish the formation of oxidized LDL-C species. Overexpression of human apolipoprotein A-I in apolipoprotein E–knockout mouse models was shown to inhibit LDL-C oxidation by 50% and reduce atherogenesis.4

HDL-C and cardiovascular risk

An inverse relationship exists between HDL-C and risk of CAD. Importantly, the risk associated with HDL-C is independent of other risk factors, including LDL-C. It has been shown that at any level of plasma LDL-C, a reduction in HDL-C increases the risk of CAD. In the PROspective CArdiovascular Münster (PROCAM) study, the risk associated with HDL-C was independent of triglyceride levels.5 In a prospective analytical study, Stampfer et al6 found that the greatest increase in cardiovascular risk associated with low HDL-C (< 47 mg/dL) was in patients with below-average total cholesterol (< 212mg/dL). Recent data from the Veterans Affairs High-density lipoprotein Intervention Trial (VA-HIT) indicate that, after correcting for other CAD risk factors, HDL-C is a predictor of CAD events. In addition, low HDL-C plasma concentrations have been shown to be a strong predictor of cardiovascular events in normocholesterolemic patients with established CAD. Results of clinical trials have reinforced the importance of addressing HDL-C levels in the prevention of CAD and its complications.

In conclusion, low HDL-C plasma levels are an independent risk factor for atherogenesis and CAD and a predictor of primary and secondary cardiovascular events.

J. C. KASKI, D. KASKI - London, UK


1. Barr DP et al. Am J Med. 1951;11:480-485. 2. Miller NE, Miller GJ. Lancet 1975;1:16-19. 3. Castelli WP et al. JAMA. 1986;256:2835-2838. 4. Hayek T et al. Eur J Clin Chem Clin Biochem. 1995;33:721-725. 5. Assmann G, Schulte H. Am J Cardiol. 1992;70:733-737. 6. Stampfer MJ et al. N Engl J Med. 1991;325:373-381.

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