Elevation of plasma lipoprotein Lp(a) above 30 mg/dL is a strong independent risk factor for coronary artery disease and possibly for stroke. A unique feature of lipoprotein Lp(a) is the structural similarity of its nonlipid moiety, apolipoprotein Lp(a), to plasminogen. This similarity allows it to bind to endothelium and to proteins of cellular membranes. It inhibits fibrinolysis by competing for plasminogen binding sites and also favors lipid deposition and stimulates smooth muscle cell proliferation. Niacin and estrogen lower lipoprotein Lp(a), but HMG CoA reductase inhibitors, fibrates, and bile acid sequestrants do not.