Oxidized low density lipoproteins (LDL) and autoimmune antibodies against oxidized LDL have been demonstrated in human atherosclerotic lesions; they may enhance the progression of these lesions by 1) enhancing monocyte adhesion and macrophage foam cell generation; 2) inducing smooth muscle cell migration, proliferation, and foam cell generation; 3) enhancing platelet adhesion and aggregation, which may stimulate macrophage foam cell generation and smooth muscle cell proliferation; 4) triggering thrombosis; and 5) impairing vasodilation, which results in increased shear stress. The oxidation of LDL probably occurs in the arterial wall, where it is sequestered from circulating antioxidants. Atherosclerotic arterial walls contain increased levels of redox‐active metal ions, and the LDL of patients with atherosclerotic cardiovascular disease are more susceptible to oxidation, possibly as a result of reduced endogenous antioxidants such as vitamin E. Dietary supplementation with vitamin E (up to 1,000 IU/day) or administration of probucol reduce the oxidation rate of LDL and may significantly decrease the risk of coronary heart disease.—Holvoet, P., Collen, D. Oxidized lipoproteins in atherosclerosis and thrombosis. FASEB J. 8, 1279‐1284 (1994)