The beneficial effect of cholesterol-lowering therapy for secondary pr
evention in patients with coronary artery disease (CAD) is well establ
ished. The therapeutic goal in this situation is a low-density lipopro
tein (LDL) cholesterol level of 100 mg/dl. Cholesterol-lowering therap
y will not only lead to a reduction in the progression of lesions but
also and probably more importantly will reduce lesion activation and r
upture and improve endothelial vasomotor function. Depending on the un
derlying hyperlipoproteinemia, the first choice for single drug therap
y is a bile acid-binding resin or a hepatic hydroxymethyl glutaryl coe
nzyme A (HMG-CoA) reductase inhibitor in isolated LDL hypercholesterol
emia, and nicotinic acid, a fibric acid, or a HMG-CoA reductase inhibi
tor in combined hyperlipidemia. Combination therapy usually consists o
f a bile acid-binding resin with ei ther an HMG-CoA reductase inhibito
r, a fibric acid, or nicotinic acid in LDL hypercholesterolemia and ni
cotinic acid with a fibric acid in combined hyperlipidemia.