[Skip to Content]
[Skip to Content Landing]
Article
February 24, 1989

Decreased Selenium Levels in Acute Myocardial Infarction

Author Affiliations

From the Department of Epidemiology, Erasmus University Medical School, Rotterdam (Drs Kok, Hofman, and Valkenburg, Ms Witteman, and Mr de Bruijn); the Department of Cardiology, Zuiderziekenhuis Hospital, Rotterdam (Dr Kruyssen); and the Department of Radiochemistry, Interuniversity Reactor Institute, Delft, the Netherlands (Dr de Bruin).

From the Department of Epidemiology, Erasmus University Medical School, Rotterdam (Drs Kok, Hofman, and Valkenburg, Ms Witteman, and Mr de Bruijn); the Department of Cardiology, Zuiderziekenhuis Hospital, Rotterdam (Dr Kruyssen); and the Department of Radiochemistry, Interuniversity Reactor Institute, Delft, the Netherlands (Dr de Bruin).

JAMA. 1989;261(8):1161-1164. doi:10.1001/jama.1989.03420080081035
Abstract

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.

(JAMA 1989;261:1161-1164)

×