Do antioxidants and polyunsaturated fatty acids have a combined association with coronary atherosclerosis?

To evaluate the antioxidant hypothesis with regard to atherosclerosis, we compared plasma selenium, serum alpha-tocopherol, serum polyunsaturated fatty acids (PUFA), and the ratios of selenium and alpha-tocopherol to PUFAs in subjects with varying degrees of coronary atherosclerosis. Cases had more than 85% stenosis in at least one coronary vessel and controls had less than 50% stenosis in all three vessels. Plasma selenium was significantly lower in cases than controls (95.1 +/- 21.0 micrograms/l and 108.8 +/- 29.3 micrograms/l, respectively). Though alpha-tocopherol and PUFA levels were similar in both groups, the ratios Se/linoleic acid, Se/total PUFA and Se/total n-6 acids were significantly lower in cases. In particular, these differences were observed in subjects with low serum alpha-tocopherol level (below the median; 1452 micrograms/dl). Moreover, in this subgroup the ratio Se/PUFA was significantly lower in cases than in controls for all PUFAs except eicosapentaenoic and docosahexaenoic acid. Though definitive conclusions cannot be drawn from our data, it is hypothesized that high PUFA levels, when insufficiently protected by antioxidants against peroxidation, may indicate a higher risk of atherosclerosis.

Decreased selenium levels in acute myocardial infarction.

To study the association between selenium status and the risk of myocardial infarction, we compared plasma, erythrocyte, and toenail selenium levels and the activity of erythrocyte glutathione peroxidase among 84 patients with acute myocardial infarction and 84 population controls. Mean concentrations of all selenium measurements were lower in cases than controls. The differences were statistically significant, except for the plasma selenium level. A positive trend in the risk of acute myocardial infarction from high to low toenail selenium levels was observed, which persisted after adjustment for other risk factors for myocardial infarction. In contrast, erythrocyte glutathione peroxidase activity was significantly higher in cases than controls (31.3 +/- 8.4 U/g of hemoglobin and 28.0 +/- 8.1 U/g of hemoglobin, respectively). Because the toenail selenium level reflects blood levels up to one year before sampling, these findings suggest that a low selenium status was present before the infarction and, thus, may be of etiologic relevance. The higher glutathione peroxidase activity in the cases may be interpreted as a defense against increased oxidant stress either preceding or following the acute event.