TY - JOUR
T1 - Prostaglandin E1 does not accelerate rTPA-induced thrombolysis in acute myocardial infarction
AU - Kleiman, Neal S.
AU - Tracy, Russell P.
AU - Schaaff, Larry J.
AU - Harris, Scott
AU - Hill, Rita D.
AU - Puleo, Peter
AU - Roberts, Robert
N1 - Funding Information:
From aBaylor College of Medicine, The Methodist Hospital, Veterans Administration Hospital, and The Ben Taub General Hospital, Houston; %he University of Vermont, Burlington; and CThe Upjohn Company, Kalamazoo. Supported by a grant from The Upjohn Company, Kalamazoo, Received for publication June 16, 1993; accepted Aug. 2, 1993. Reprint requests: Neal S. Kleiman, Section of Cardiology, Baylor College of Medicine, The Methodist 6535 Fannin, MS F-905, Houston, TX 77030.
Copyright:
Copyright 2018 Elsevier B.V., All rights reserved.
PY - 1994/4
Y1 - 1994/4
N2 - Fitteen patients who arrived between 6 and 24 hours after the onset of acute myocardial infarction and who were found to have totally occluded coronary arteries, received aspirin, heparin, and tissue plasminogen activator given over 3 hours. Eight patients were randomly assigned to receive intravenous prostaglandin E1, 20 ng/kg/min for 6 hours, while 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 two of eight (25%) patients treated with prostaglandin E1 and in two of seven (28%) patients receiving placebo. Pharmacologic sampling of tissue plasminogen activator levels were performed at baseline and 30, 45, 60, 75, 90, 135, 180, 190, 210, and 240 minutes afterwards for assessment of tissue plasminogen activator antigen. There was no difference in fibrinogen levels and no difference in tissue plasminogen activator antigen levels at these time periods. Clearance values of tissue plasminogen activator were calculated and were not different between the two groups. These data do not support the use of prostaglandin E1 for the acceleration of reperfusion in patients receiving tissue plasminogen activator for acute myocardial infarction.
AB - Fitteen patients who arrived between 6 and 24 hours after the onset of acute myocardial infarction and who were found to have totally occluded coronary arteries, received aspirin, heparin, and tissue plasminogen activator given over 3 hours. Eight patients were randomly assigned to receive intravenous prostaglandin E1, 20 ng/kg/min for 6 hours, while 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 two of eight (25%) patients treated with prostaglandin E1 and in two of seven (28%) patients receiving placebo. Pharmacologic sampling of tissue plasminogen activator levels were performed at baseline and 30, 45, 60, 75, 90, 135, 180, 190, 210, and 240 minutes afterwards for assessment of tissue plasminogen activator antigen. There was no difference in fibrinogen levels and no difference in tissue plasminogen activator antigen levels at these time periods. Clearance values of tissue plasminogen activator were calculated and were not different between the two groups. These data do not support the use of prostaglandin E1 for the acceleration of reperfusion in patients receiving tissue plasminogen activator for acute myocardial infarction.
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U2 - 10.1016/0002-8703(94)90539-8
DO - 10.1016/0002-8703(94)90539-8
M3 - Article
C2 - 8154410
AN - SCOPUS:0028411612
VL - 127
SP - 738
EP - 743
JO - American Heart Journal
JF - American Heart Journal
SN - 0002-8703
IS - 4 PART 1
ER -