PROSTAGLANDIN EL DOES NOT ACCELERATE RTPA-INDUCED THROMBOLYSIS IN ACUTE MYOCARDIAL-INFARCTION

Fifteen patients who arrived between 6 and 24 hours after the onset of acute myocardial infarction and who were found to have totally occlud ed coronary arteries, received aspirin, heparin, and tissue plasminoge n activator given over 3 hours. Eight patients were randomly assigned to receive intravenous prostaglandin E(1), 20 ng/kg/min for 6 hours, w hile seven patients received placebo infusion. Coronary arteriography begun immediately before the start of tissue plasminogen activator and repeated every 15 minutes revealed restoration of antegrade flow in t wo of eight (25%) patients treated with prostaglandin E(1) and in two of seven (28%) patients receiving placebo. Pharmacologic sampling of t issue plasminogen activator levels were performed at baseline and 30, 45, 60, 75, 90, 135, 180, 190, 210, and 240 minutes afterwards for ass essment of tissue plasminogen activator antigen. There was no differen ce in fibrinogen levels and no difference in tissue plasminogen activa tor antigen levels at these time periods. Clearance values of tissue p lasminogen activator were calculated and were not different between th e two groups. These data do not support the use of prostaglandin E(1) for the acceleration of reperfusion in patients receiving tissue plasm inogen activator for acute myocardial infarction.