There seems little doubt that triglycerides are causally related to the progress of atherogenesis. Mechanisms for this effect include adverse quantitative and qualitative changes in circulating lipoproteins. In particular, the effects of lower high-density lipoprotein levels and the production by hypertriglyceridemia of small, dense low-density lipoproteins are of great significance. The role of triglyceride-rich remnant particles in atherogenesis is likely important. These remnants, which are lipoproteins rich in both cholesterol and triglycerides, can be shown to produce cholesteryl ester—laden macrophages in vitro and are probably atherogenic in vivo. Triglyceride levels are a significant risk factor for coronary artery disease in women, more so than in men. Triglyceride levels also increase in older patients and continue to be predictors of coronary risk in both men and women older than 65 years. It is unclear whether triglyceride intervention efforts should be directed at lowering triglyceride levels (such as is accomplished with niacin or fibric acid derivatives) or lowering low-density lipoprotein levels in patients with high triglyceride levels, assuming triglyceride levels are only a passive marker of atherosclerotic risk. Until more is known about the precise role of hypertriglyceridemia in atherogenesis in women and older patients, use of triglyceride-lowering drugs should be conservative and limited to those individuals with high triglyceride levels (>4.5 mmol/L [ >400 mg/dL]) who do not respond to diet modifications and who are at risk of coronary disease either because of a history of vascular disease or the presence of other risk factors.
Arch Intern Med. 1997;157:961-968
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