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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.
[QUOTE=ARIZONA73]Interesting. I know that a lot of people, out of desperation, jump on the low-fat bandwagon. I've seen a comparison study pitting the Ornish diet against the Atkins diet. Although the Ornish diet was more effective at lowering TC and LDL, the Atkins diet was overwhelmingly more effective at raising HDL and lowering triglycerides. So, I think if I had to choose one or the other, I'd certainly favor the Atkins diet, or any other low-carb diet. If Ornish is that skinny, it's no wonder. When it comes to meals, what is there to get excited about? Who wants to eat like a rabbit for the rest of their life?[/QUOTE]

:yawn: That's true Arizona. I don't enjoy most of the food i eat right now (like a rabbit) but i do enjoy the benefits. i eat high fiber and low fat meals most days. Sad but true, i eat just about the same thing everyday and for each meal. I've lost a lot of weight, and my glucose levels have dropped, my bp dropped, but not stable yet. I hope when i see my endo 7-29 he tells me my cholesterol has dropped too.

I purchased a cookbook for low fat meals. I hate it, but this is my life for now. My hubby is no help either, he eats all the GOOD, GREASY foods, while i munch on celery and carrot sticks. Atkins diet would be a :nono: :nono: for me.

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