Tissue damage in acute myocardial infarction: selective protection by vitamin E.

A growing amount of scientific evidence supports the participation of oxygen radicals in heart disease and, consequently, a protective effect of vitamin E (VE), beta-carotene (BC), and other antioxidants. The aim of this study was to correlate plasma VE and BC concentration with the clinical course of the acute myocardial infarction (AMI). We evaluated 120 patients that were admitted at the coronary units within 12 h after the development of AMI symptoms. The AMI was diagnosed by clinical and biochemical criteria and by electrocardiography and echocardiography. Plasma VE and BC concentration was determined by high performance liquid chromatography. The patients were separated according to the plasma concentration of VE (group H, VE > 17.5 microM; group L, VE < 17.5 microM). Clinical history of patients, age, sex, associated cardiovascular risk factors, AMI localization, hemodynamic class, and the treatment received were similar between different groups. The blood levels of creatine phosphokinase (CK) evaluated either 24- or 48-h after admittance, were higher in group L than in group H (24 h: H = 436 +/- 31 U/ml vs. L = 642 +/- 84 U/ml; p < .005; 48 h: H = 242 +/- 21 U/ml; L = 423 +/- 82 U/ml, p < 0.005). The number of deflexions in the electrocardiogram at admittance (ECG-D) was significantly higher in group L than in group H (4.7 +/- 0.3 vs. 3.7 +/- 0.2; p < .005). The number of new Q waves in the ECG of release (ECG-Q) was higher in group L than in group H (2.9 +/- 0.3 vs. 2.2 +/- 0.2; p < .05). The number of segments affected in the echocardiograms (EC-S) was: L = 5.3 +/- 0.6 vs. H = 4.4 +/- 0.2; p = 0.11. No significant differences in CK levels, ECG-D, ECG-Q, and EC-S were observed when the patients were separated according their plasma BC levels. These results indicate that a high concentration of plasma VE, but not BC, was associated with a diminution in the creatine phosphokinase release and with the AMI extension.