Cardiovascular event reduction in hypercholesterolemic subjects appropriately emphasizes the prominent role of statin therapy; however, niacin (nicotinic acid) is also an effective lipid-altering agent that prevents atherosclerosis and reduces cardiovascular events. Niacin has multifarious lipoprotein and anti-atherothrombosis effects that improve endothelial function, reduce inflammation, increase plaque stability, and diminish thrombosis. Niacin reduces the atherogenicity of low-density lipoprotein (LDL) by changing the distribution of small LDL to large LDL subclass, and the susceptibility of LDL to oxidative modification. It is the most effective agent for increasing high-density lipoprotein cholesterol. Moreover, it favorably alters high-density lipoprotein composition, increasing apolipoprotein AI relative to apolipoprotein AII. Niacin reduces blood viscosity through a variety of mechanisms, thus improving blood flow and perfusion through stenotic segments of the vasculature. Finally, niacin has cardioprotective effects that may limit ischemia-reperfusion injury. By preserving glycolysis during periods of ischemia and improving subendocardial blood flow during reperfusion, niacin can improve the functional recovery of the myocardium.