Abstract
Postprandial hyperlipidemia has been associated with cardiovascular disease and is recognized as a coronary artery disease risk factor. The mechanisms underlying this association depend on a multitude of effects. Cholesterol-enriched, atherogenic remnants of chylomicrons accumulate in the postprandial state. These remnants readily induce foam cell formation in cultured macrophages and smooth muscle cells, and endothelial cell function is compromised by increased remnant concentrations. Conventional lipid-lowering drugs such as statins and fibrates reduce postprandial hyperlipidemia. However, the contribution of decreased postprandial lipoproteins to the atheroprotection associated with these agents has not been elucidated. Newer agents, including isoform-specific acyl-CoA:cholesterol acyltransferase inhibitors, inhibitors of cholesterol absorption, plant sterols and stanols, and selective microsomal triglyceride transfer protein inhibitors may play a role in attenuating postprandial hyperlipidemia. These novel treatments will need to be assessed for efficacy in addition to their ability to decrease coronary artery disease risk.
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