LP(a) lipoprotein, discovered by Berg, appears as an independent risk factor for atherogenesis with a weight similar to that of the total to HDL cholesterol ratio. It is probably synthesized in the liver and its metabolism is similar to that of LDL; however degradation is preferential mediated by monocytes and macrophages. It is structurally related to plasminogen and may interfere with fibrinolysis. In vitro, its atherogenic power surpasses that of LDL. Elevated levels of LP(a) are inherited as an autosomic codominant trait. Increased atherogenic risk, both at coronary and cerebrovascular sites, is associated to plasma LP(a) levels in excess of 20 mg/dl. Its plasma level increases during pregnancy, after menopause, with renal failure and in decompensated insulin dependent diabetes. Plasma levels are decreased by stanozolol and chronic alcoholism. Diet therapy is of no value for control of high LP(a) levels; only neomycin associated to nicotinic acid has proven effective.