Emerging importance of HDL cholesterol in developing high-risk coronary plaques in acute coronary syndromes.
Cardiovascular disease is the principal cause of death in industrialized countries. Hyperlipidemia, with high low-density lipoprotein cholesterol and triglycerides, and low high-density lipoprotein cholesterol levels (<40 mg/dL in men and <45 mg/dL in women), is a known major cardiovascular risk factor. Statins are considered the most potent and effective agents to reduce low-density lipoprotein cholesterol, but they have a variable effect on high-density lipoprotein cholesterol and triglycerides. Different clinical trials with statins have shown a decrease in low-density lipoprotein cholesterol by 35% and a reduction of the incidence of coronary events by as much as 30%. However, 60 to 70% of events still occur, despite remarkable reduction of low-density lipoprotein cholesterol concentration. Recent National Cholesterol Education Program guidelines highlighted the importance of high-density lipoprotein cholesterol concentration in the prevention and treatment of cardiovascular disease. High-density lipoprotein cholesterol is considered an independent risk factor and has an inverse relation with coronary events. The association of low levels of high-density lipoprotein cholesterol with an increased incidence of cardiovascular events implies a critical role of high-density lipoprotein in the protection against atherosclerotic disease and in the progression of coronary atherosclerotic disease. High-density lipoprotein cholesterol appears to exert this protective effect through multiple mechanisms. High-density lipoprotein is not only involved in reverse cholesterol transport, but also prevents endothelial dysfunction; inhibits the homing of monocytes, apoptosis, platelet activation, and factor X activation; and has antioxidant properties. In this article the authors review the available experimental and clinical evidence supporting the importance of high-density lipoprotein cholesterol as a protective factor in coronary artery disease, and the strategies developed to increase high-density lipoprotein cholesterol.
Viles-Gonzalez
Juan F
JF
Cardiovascular Biology Research Laboratory, Zena and Michael A Weiner Cardiovascular Institute, Mount Sinai School of Medicine, New York, New York 10029, USA.
Fuster
Valentin
V
Corti
Roberto
R
Badimon
Juan J
JJ
D000818:Animals; D008076:Cholesterol, HDL / Q000502:physiology*; D003324:Coronary Artery Disease / Q000097:blood / Q000503:physiopathology* / Q000517:prevention & control; D003327:Coronary Disease / Q000097:blood / Q000503:physiopathology*; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000503:physiopathology; D015248:Gemfibrozil / Q000627:therapeutic use; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D015539:Platelet Activation / Q000502:physiology
D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D015248:Gemfibrozil