RECOMBINANT HUMAN SUPEROXIDE-DISMUTASE (H-SOD) FAILS TO IMPROVE RECOVERY OF VENTRICULAR-FUNCTION IN PATIENTS UNDERGOING CORONARY ANGIOPLASTY FAR ACUTE MYOCARDIAL-INFARCTION

Background Animal studies have demonstrated a burst of oxygen free radical generation after reperfusion of ischemic myocardium that could be blocked by administration of the free radical scavenger recombinant human superoxide dismutase (h-SOD). A multicenter, randomized, placebo-controlled clinical trial was designed to test the hypothesis that free radical-mediated reperfusion injury could be reduced by intravenous administration of h-SOD begun before percutaneous transluminal coronary angioplasty (PTCA) in patients with acute transmural myocardial infarction. Methods and Results One hundred twenty patients were randomized to receive placebo (n=59) or h-SOD (n=61) given as a 10-mg/kg intravenous bolus followed by a 60-minute infusion of 0.2 mg . kg(-1) . min(-1). Left ventricular function was analyzed via paired contrast left ventriculograms performed before PTCA and after 6 to 10 days and paired radionuclide ventriculograms performed within 24 hours of PTCA and after 4 to 6 weeks. Both h-SOD- and placebo-treated patients showed improvement in global and regional left ventricular function after successful reperfusion. Compared with the placebo group, no additional improvement was observed in the patients treated with hSOD. Conclusions The results of this clinical trial failed to demonstrate a beneficial effect of h-SOD on global or regional left ventricular function in patients who underwent successful PTCA for treatment of acute myocardial infarction.