Effects of nonstatin lipid drug therapy on high-density lipoprotein metabolism

Abstract

Low high-density lipoprotein (HDL) cholesterol is an important predictor of risk for coronary artery disease. Although current treatment guidelines for dyslipidemia do not include specific targets for HDL cholesterol, the categorical definition of low HDL cholesterol has been changed from <35 mg/dL to <40 mg/dL. 3-hydroxy-3-methylglutaryl reductase inhibitors (statins) increase HDL cholesterol to a moderate degree. Fibrates also increase HDL cholesterol to a moderate degree and have additive effects with statins. Niacin is the most potent currently available agent for increasing HDL cholesterol, and its effects are also additive to those of statins. Other agents that increase HDL cholesterol include thiazolidinediones, estrogen, and omega-3 fatty acids. The mechanisms by which nonstatin pharmacologic agents increase HDL cholesterol are not completely understood but probably involve multiple mechanisms for each class.