If triglyceride-rich very-low-density lipoproteins (VLDLs) are a vehicle for transporting cholesterol into the arterial wall, they can be equated to low-density lipoproteins (LDLs) in estimating CHD risk and setting targets for therapy. Furthermore, the fate of cholesterol-rich VLDL (VLDL remnants) is similar to that of LDL; that is, both are removed from the circulation via LDL receptors. Thus, combining VLDL and LDL into a common category of atherogenic lipoproteins provides a rational framework for treatment of hypercholesterolemic patients with hypertriglyceridemia. A hydroxymethylglutaryl coenzyme A reductase inhibitor may be the best choice for treatment when both triglyceride and cholesterol levels are elevated, because these agents cause the greatest reduction in VLDL and LDL cholesterol levels. When hypertriglyceridemia is severe, a fibric acid or nicotinic acid is preferable, because these agents are more effective for lowering triglyceride levels and hence for reducing risk for acute pancreatitis.
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