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Targeting triglycerides as a vascular risk factor is justified because of the role of triglyceride-rich lipoproteins in atherogenesis. This review examines recent evidence connecting triglycerides with cardiovascular disease (CVD) in the context of advances in insights concerning the pathophysiology, population burden and prognostic impact of fasting versus nonfasting values.Cross-sectional surveys indicate that mean triglyceride levels in the United States have increased in recent decades. Although elevated fasting triglycerides are consistently associated with increased CVD risk, adjustment for other risk factors (especially high-density lipoprotein cholesterol (HDL-C)) substantially attenuates this relationship. A recent meta-analysis of 27 prospective studies of western populations reported a triglyceride impact on CVD in both sexes, for both fasting and nonfasting values. Nonfasting triglycerides maintained an independent graded relationship with CVD in fully adjusted analyses, with elevated 4 h postprandial triglyceride imposing a 4.5-fold increment relative to lower levels.Evidence supports a potential role for both fasting and nonfasting triglycerides as vascular risk factors, owing in part to the accompanying burden of atherogenic remnant particles, small dense low-density lipoprotein, reduced HDL-C and a high frequency of accompanying insulin resistance. Triglyceride-associated CVD risk occurs even in patients with low low-density lipoprotein cholesterol (LDL-C), and lowering both lipids provides more benefit than reducing LDL-C alone.