Tissue damage in acute myocardial infarction: Selective protection by vitamin E

A growing amount of scientific evidence supports the participation of oxyge n radicals in heart disease and, consequently, a protective effect of vitam in E (VE), beta-carotene (BC), and other antioxidants. The aim of this stud y was to correlate plasma VE and BC concentration with the clinical course of the acute myocardial infarction (AMI). We evaluated 120 patients that we re 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 w as determined by high performance liquid chromatography. The patients were separated according to the plasma concentration of VE (group fl, VE > 17.5 mu M; group L, VE < 17.5 mu M). Clinical history of patients, age, sex, ass ociated cardiovascular risk factors, AMI localization, hemodynamic dass, an d the treatment received were similar between different groups. The blood l evels of creatine phosphokinase (CK) evaluated either 24-or 48-h after admi ttance, were higher in group L than in group H (24 h: H = 436 +/- 31 U/ml v s. 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 admi ttance (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 rel ease (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 differ ences 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 tha t a high concentration of plasma VE, but not BC, was associated with a dimi nution in the creatine phosphokinase release and with the AMI extension. (C ) 1999 Elsevier Science Inc.