Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor (statin) therapy have demonstrated improvement in coronary atherosclerosis progression and reduction in risk of cardiovascular events. However, improvement in cardiovascular end-points is incompletely explained by the baseline or treated LDL cholesterol level. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify hemostasis. Local activation of platelets and thrombus formation adjacent to atheromatous plaques, especially where ruptured or eroded, are now recognized to be of pathophysiological importance in the acute and chronic clinical expression of coronary heart disease. Thus, favorable effects of statins on hemostasis may be relevant to decreasing or delaying the progression and clinical manifestations of atherosclerosis.