THERAPY AND PREVENTION

Three hundred sixty-eight patients were randomly assigned to receive intravenous streptokinase (IVSK) (n = 191) or standard therapy (n = 177) to determine the efficacy of IVSK in the treatment of acute myocardial infarction. The mean time to treatment was 3.5 hr. At 14 days there were 12 deaths in the treatment group (6.3%) and 17 deaths in the control group (9.6%) (p = .23). Early mortality was related to infarct location. Fourteen day mortality for anterior infarctions was 10.4% for treatment with IVSK and 22.4% for control patients (p = .06) and was similar for IVSK-treated patients with inferior infarctions, 4.0% vs 1.8% (p = .32). For those randomized under 3 hr, 14 day mortality tends to be lower in treated patients, 5.2% vs 11.5% (p = .11). There was significant improvement in long-term survival for patients with anterior infarction; 2 year survival was 81% for IVSK-treated patients and 65% for control patients (p = .05). There was no improvement in survival for patients with inferior myocardial infarction (p = .27). We conclude that patients with anterior myocardial infarction have improved survival when treated within the first 6 hr of symptoms. Patients with inferior infarction do not appear to have improved survival with thrombolytic therapy. Some of this improvement in survival in patients with anterior infarction may be due to a higher frequency of revascularization procedures in the treatment group. Circulation 77, No. 2, 345-352, 1988. THROMBOLYTIC THERAPY for acute myocardial infarction became possible in the early part of this decade with the demonstration of the important role of coronary artery thrombosis as the immediate cause of acute myocardial infarction.1 Early reports from Russia and West Germany demonstrated the efficacy of intracoronary streptokinase in achieving coronary artery reperfusion in the setting of acute infarction.2 3 After reports of numerous pilot studies, two small randomized trials of intracoronary streptokinase were reported,4demonstrating coronary artery reperfusion rates between 65% and 85%. Those that began streptokinase therapy within 3 hr of the onset of chest pain demonstrated evidence of myocardial salvage with an increase in ejection fraction and improved regional wall motion in the treated patients.5 These initial trials From the Department of Medicine, Division of Cardiology, University of Washington, Seattle. The trial was supported in part by the W. M. Keck Foundation, grant HL 30300 from the National Heart, Lung, and Blood Institute, National Institutes of Health, and by the General Medical Research Fund of the Seattle Veterans Administration Medical Center. Address for correspondence: J. Ward Kennedy, M.D., Director, Division of Cardiology, Mail Stop RG-22, University of Washington, Seattle, WA 98195. Received June 5, 1987; revision accepted Oct. 22, 1987. Vol. 77, No. 2, February 1988 were too small to define adequately the effect of intracoronary streptokinase on survival. Two larger studies have shown a significant reduction in early mortality.6' 7 These results of intracoronary streptokinase, as well as the knowledge that intracoronary therapy was not feasible for many patients and delayed the onset of treatment, led us to study intravenous streptokinase (IVSK) in the treatment of acute myocardial infarction. This trial was planned in the spring of 1982 and funded in August 1983, and patients were entered between September 1983 and August 1986.