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VIEWPOINT

Antioxidants, statins, and atherosclerosis

^* Weill Medical College of Cornell University, New York, New York, USA

Manuscript received June 25, 2002; revised manuscript received December 11, 2002, accepted December 25, 2002.

^* Reprint requests and correspondence: Dr. Antonio M. Gotto, Jr, c/o Mr. Jesse Jou, Weill Medical College of Cornell University, 445 East 69th Street, Olin Hall 205, New York, New York 10021, USA.
amg_editorial{at}med.cornell.edu

Research into the oxidation of lipoproteins has yielded many new insights into the pathogenesis of atherosclerosis. However, despite lipoprotein oxidation’s biologically plausible role in atherogenesis, several studies have reported inconsistent effects of antioxidants on clinical coronary end points, in sharp contrast with the studies of lipid modification with the 3-hydroxy-3-methylglutaryl coenzyme A inhibitors, or statins. There appears to be little support for the use of antioxidants in coronary prevention. However, the picture remains incomplete. What are the limitations of available antioxidant studies and the agents used? Until the picture can be clarified, lipid modification with strategies proved to reduce the risk for coronary events, such as statins or dietary changes in the style of the Mediterranean diet, should be better implemented in clinical practice.

Abbreviations and Acronyms   ASAP = Antioxidant Supplementation in Atherosclerosis Prevention study   ATBC = Alpha-Tocopherol-Beta-Carotene cancer prevention study   CAD = coronary artery disease   CHAOS = Cambridge Heart AntiOxidant Study   HATS = High-density lipoprotein Atherosclerosis Treatment Study   HDL-C = high-density lipoprotein cholesterol   LDL = low-density lipoprotein   LDL-C = low-density lipoprotein cholesterol   MI = myocardial infarction   MVP = MultiVitamins and Probucol study   SPACE = Secondary Prevention with Antioxidants of Cardiovascular disease in End-stage renal disease study

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