Author + information
- Received January 19, 1994
- Revision received June 1, 1994
- Accepted June 13, 1994
- Published online November 15, 1994.
- Laurent Sebbag, MDa,
- Rémi Forrat, MDa,
- Emmanuelle Canet, DVMa,
- Serge Renaud, PhDa,
- Jacques Delaye, MD∗ and
- Michel de Lorgeril, MD∗,a
- ↵∗Address for correspondence: Dr. Michel de Lorgeril, INSERM U.63, 22 avenue Doyen Lépine, 69500 Bron, France.
Objectives. We investigated whether dietary supplementation with the antioxidant vitamin alpha-tocopherol (500 mg daily) might reduce lethal ventricular arrhythmias and infarct size.
Background. Previous studies suggested that dietary supplementation with alpha-tocopherol may be associated with a reduced risk of ischemic heart disease. However, the mechanism of this protection remains unknown.
Methods. Beagle dogs were randomized to either a supplemented or a control group. Because of the low mortality rate in the supplemented group, five dogs were added to the control group. After 2 months, dogs were anesthetized and underwent a 2-h coronary artery occlusion and 6-h reperfusion. Plasma vitamin E, retinol and malondialdehyde concentrations were assessed in all dogs.
Results. Fourteen dogs (11 of 25 control vs. 3 of 19 supplemented dogs, p < 0.05) developed ventricular fibrillation during either ischemia or reperfusion. Malondialdehyde concentrations were higher in dogs that subsequently developed arrhythmias (2.7 ± 0.2 μmol/liter, mean ± SEM) compared with dogs that did not (2.1 ± 0.2 μmol/liter, p = 0.03). Among survivors with significant ischemia, infarct size was larger in supplemented (n = 12, 58.5 ± 3.3% of area at risk) than in control (n = 11, 41.9 ± 6.5%, p < 0.04) dogs. In addition, for a given collateral flow, supplemented dogs (n = 16) developed larger infarct size than control dogs (n = 15, p < 0.001, analysis of covariance).
Conclusions. The data suggest that dietary alpha-tocopherol supplementation prevented lethal ventricular arrhythmias associated with ischemia and reperfusion. However, its influence on infarct size and long-term prognosis warrants further investigation.
☆ This study was supported in part by grants from INSERM and Lyon Pharmaceutique Laboratory, Lyon, France.
- Received January 19, 1994.
- Revision received June 1, 1994.
- Accepted June 13, 1994.
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