Abstract
Epidemiological studies have identified high-density lipoproteins (HDLs) and triglycerides (TGs) as independent risk factors that modulate cardiovascular disease (CVD) risk (1). During the past decade, clinical trials of low-density lipoprotein (LDL)-lowering drugs have clearly established that reductions in LDL are associated with a 30 to 45% reduction in clinical events. However, despite lowered LDL levels, many patients continue to have cardiac events. This implies that a greater improvement could be achieved through further interventional measures, including therapy that modifies lipids other than LDL. Indeed, low HDL and high TG levels are often present in high-risk patients with CVD. In fact, a low level of HDL-cholesterol (C), rather than a high level of LDL-C, is currently the most common lipid abnormality in patients with coronary artery disease (CAD) in the United States. As a result, a great deal of research interest recently has been focused on raising plasma HDL levels as well as lowering TG levels by dietary, pharmacological, or genetic manipulations, as a potential strategy for the treatment of CVD. In addition to epidemiological studies, other lines of evidence suggest that modifying HDL and TG levels would reduce the risk of CVD.
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References
Barr DB, Russ EM, Eder HA. Protein-lipid relationship in human plasma: II. In atherosclerosis and related conditions. Am J Med 1951;11:480–493.
Goffman JW, Young W, Tandy R. Ischemic heart disease, atherosclerosis, and longevity. Circulation 1966;34:679–697.
Castelli WP, Garrison RJ, Wilson WF, et al. Incidence of coronary heart disease and lipoprotein cholesterol levels: the Framingham Study. JAMA 1986;256:2835–2838.
Secondary prevention by raising HDL cholesterol and reducing triglyceride in patients with coronary artery disease: the Bezafibrate Infarction Prevention Study. Circulation 2000, July 4;102:21–27.
Family Study Committee for the Lipid Research Clinics Program. The collaborative Lipid Research Clinics Program Family Study. I. Study design and description of data. Am J Epidemiol 1984;119:931–943.
Family Study Committee for the Lipid Research Clinics Program Family Study. The collaborative Lipid Research Clinics Program Family Study. Bivariate path analysis of lipoprotein concentration. Genet Res 1983;42:117–135.
Lipid Research Clinics Program. The Lipid Research Clinics Coronary Primary Prevention Trial results. II. The relationship of reduction in incidence of coronary heart disease to cholesterol lowering. JAMA 1984;251:365–374.
Namboodiri KK, Green PP, Kaplan EB, et al. Family aggregation of high density lipoprotein cholesterol. Collaborative Lipid Research Clinics Program Family Study. Arteriosclerosis 1983;3:616–626.
Miller NE, Thelle DS, Forde OH, Mjos OD. The Tromso heart-study. High-density lipoprotein and coronary heart-disease: a prospective case-control study. Lancet 1977;1:965–968.
Assmann G, Schulte H. Role of triglycerides in coronary artery disease: lessons from the Prospective Cardiovascular Muenster Study. Am J Cardiol 1992;70:10H–13H.
Assman G, Schulte H. Obesity and hyperlipidemia: results from the Prospective Cardiovascular and Muenster (PROCAM) study. In: Bjorntorp P, Brodoff B, eds. Obesity. JB Lippincott, New York, 1992, pp. 502–511.
Fontbonne A, Charles MA, Thilbult N, et al. Hyperinsulinemia as a predictor of coronary heart disease mortality in a healthy population: The Paris Prospective Study, 15 year follow-up. Diabetologia 1991;34:356–361.
Manninen V, Tenkanen L, Koskinen P, Huttunen JK, et al. Joint effects of serum triglycerides and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helskinki Heart Study implications for treatment. Circulation 1992;85:37–45.
Rubins HB, Robins SJ, Collins D, et al. Gemfibrozil for the secondary prevention of coronary heart disease in men with low levels of high-density lipoprotein cholesterol. Veterans Affairs High-Density Lipoprotein Cholesterol Intervention Trial Study Group. N Engl J Med 1999;341:410–418.
Nissen SE, Tsunoda T, Tuzcu EM, et al. Effect of recombinant ApoA-I Milano on coronary atherosclerosis in patients with acute coronary syndromes: a randomized controlled trial. JAMA 2003;290:2292–2300.
Brousseau ME, Schaefer EJ, Wolfe ML, et al. Effects of an inhibitor of cholesteryl ester transfer protein on HDL cholesterol. N Engl J Med 2004;350:1505–1515.
Clark RW, Sutfin TA, Ruggeri RB, et al. Raising high-density lipoprotein in humans through inhibition of cholesteryl ester transfer protein: an initial multidose study of torcetrapib. Arterioscler Thromb Vasc Biol 2004;24:490–497.
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© 2006 Humana Press Inc., Totowa, NJ
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Foody, J.M. (2006). High-Density Lipoprotein Cholesterol, Triglycerides, and Coronary Artery Disease. In: Foody, J.M. (eds) Preventive Cardiology. Contemporary Cardiology. Humana Press. https://doi.org/10.1007/978-1-59745-096-6_5
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DOI: https://doi.org/10.1007/978-1-59745-096-6_5
Publisher Name: Humana Press
Print ISBN: 978-1-58829-521-7
Online ISBN: 978-1-59745-096-6
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