Randomized double-blind trial of intravenous streptokinase for acute myocardial infarction

• Published in: The American journal of cardiology Vol. 58; no. 1; pp. 47 - 52
• Main Authors: Schreiber, Theodore L., Miller, David H., Silvasi, Denise A., Moses, Jeffrey W., Borer, Jeffrey S.
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.07.1986; Elsevier
• Subjects: Adult; Aged; Antianginal agents. Coronary vasodilator agents; Biological and medical sciences; Cardiovascular system; Clinical Trials as Topic; Double-Blind Method; Female; Heart - drug effects; Heart - physiopathology; Humans; Injections, Intravenous; Male; Medical sciences; Middle Aged; Myocardial Infarction - drug therapy; Myocardial Infarction - physiopathology; Pharmacology. Drug treatments; Random Allocation; Streptokinase - administration & dosage; Streptokinase - therapeutic use; Stroke Volume - drug effects; Human; Drug; Intravenous administration; Infarct; Enzyme; Acute; Cardiovascular disease; Coronary heart disease; Chemotherapy; Streptokinase; Placebo; Double blind study; Myocardium; Fibrinolytic
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/0002-9149(86)90239-0

To determine the efficacy of intravenously administered streptokinase (SK) on infarct artery patency, global left ventricular (LV) function and clinical course in transmural acute myocardial infarction (AMI), 38 patients were studied using a randomized, double-blind, placebo-controlled scheme. Nineteen patients received 1.0 million units of SK followed by 72 hours of heparin infusion and 19 received placebo followed by heparin infusion, all within 5 hours (mean 3.3 hours) after AMI onset. Patients ineligible for inclusion in the randomized trial were followed as a second, “historical control” group. Compared with placebo, SK caused a higher frequency of enzymatic evidence of reperfusion (6% vs 79%, p < 0.001) and of patent infarct-related arteries at predischarge coronary arteriography (64% vs 88%, difference not significant). (Patients in the control group had a relatively low frequency of spontaneous thrombolysis—28%.) In the SK group LV ejection fraction increased from early (average 7.3 hours after AMI) to late (predischarge) study (from 40% early to 47% late, p < 0.05); in the placebo group LV ejection fraction did not change significantly (from 41% to 42%). Predischarge exercise radionuclide ventriculography showed mild and similar degrees of inducible ischemia in both groups. After a mean of 12.8 months of follow-up, 1 SK patient and 4 placebo patients had died (difference not significant). In conclusion, intravenous SK is efficacious for thrombolysis in patients with AMI. It improves global LV function without augmenting exercise-inducible ischemia.