A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex) in acute myocardial infarction: The Duke University clinical cardiology study (DUCCS) 1

Christopher M. O'Connor, Roderick Meese, Robert Carney, Jack Smith, Eric Conn, John Burks, Carl Hartman, Steve Roark, Neal Shadoff, Maurice Heard, Brant Mittler, Gary Collins, Frank Navetta, Jeff Leimberger, Kerry Lee, Robert M. Califf

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55 Scopus citations

Abstract

Objectives. We designed a randomized trial to evaluate the effects of heparin administration in conjunction with anistreplase (anisoyiated plasminogen streptekinase activator complex [APSAC]) on arterial patency and clinical end points. Background. The role of conjunctive intravenous heparin therapy with APSAC has not been tested despite the recommendations that intravenous heparin should be used. Methods. Four hours after APSAC administration, 250 patients with acute myocardial infarction were randomly assigned to receive 325 mg of either aspirin alone or aspirin and a continuous infusion of heparin (15 IU/kg body weight per h). Clinical ischemic events and bleeding complications were monitored On hospital day 5, coronary arteriography and left veetriculography were performed. Results. The primary end point of the trial (the combined outcome of death, reinfarction, recurrent ischemia and occlusion of the infarct-related artery) occurred in 42% of the heparin-treated group versus 43% of the group without heparin (p = 0.94). A patent infarct-related artery was present in 80% of the treated with heparin and in 73% of those treated without heparin (p = 0.26). Left ventricular function, as measured by ejection fraction, was well preserved in both groups (52% vs. 50.5%, respectively, p = 0.29). The overall bleeding rate was higher in patients with (32%) than without (17.2%) heparin (p = 0.006). Conclusions. Weight-adjusted intravenous heparin therapy after APSAC in acute myocardial infarction does not reduce the combined incidence of death, reinfarction, recurrent ischemia and ccclusion of the infarct-related artery. Furthermore, withholding intravenous heparin therapy is associated with a 46% reduction in bleeding complications. Our findings do not support the addition of intravenous heparin after APSAC therapy, as currently recommended, and suggest that a strategy of withholding heparin is simpler and safer and does not place the patient at increased risk for ischemic complications after myocardial infarction.

Original languageEnglish
Pages (from-to)11-18
Number of pages8
JournalJournal of the American College of Cardiology
Volume23
Issue number1
DOIs
StatePublished - Jan 1994

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