Author + information
- Received May 22, 1992
- Revision received December 21, 1992
- Accepted February 9, 1993
- Published online August 1, 1993.
- Frans Van De Werf, MD, FACC∗,1,
- Luc Janssens, MD1,
- Thomasz Brzostek, MD1,
- Luc Mortelmans, MD1,
- J.T.H. Wackers, MD, FACC∗,
- Georges M. Willems, PhD†,
- Hein HeidbÜchel, MD1,
- Emmanuel Lesaffre, DrSc1,
- Ilse Scheys, MSc1,
- Désiré Collen, MD, PhD1 and
- Hilaire De Geest, MD1
- ↵∗Address for correspondence: Frans Van de Werf, MD, Department of Cardiology, University Hospital Gasthuisberg, Herestraat 49, B-3000 Leuven, Belgium.
Objectives. This study was conducted to explore mechanisms that could explain the possible clinical benefit of early administration of a beta1-selective adrenoreceptor blocking agent or a bradycardiac drag as adjunct to thrombolysis in acute myocardial Infarction.
Background. The effects of beta-blockers given concomitantly with thrombolytic therapy in patients with acute myocardial infarction have not been fully examined. The potential role of specific bradycardiac agents lacking negative inotropism as an alternative to beta-blockers in this setting has never been studied in humans.
Methods. In a double-blind study, we examined the effects of early intravenous and continued oral administration of a beta-blocker (atenolol), a specific bradycardiac (alinidine) or placebo on left ventricular function, late coronary artery patency, infarct size, exercise capacity and incidence of arrhythmias.
Results. A total of 292 patients with acute myocardial infarction of ≤ 5 h duration and without contraindications to thrombolytic or beta-blocker therapy were studied. Of these, 100 were allocated to treatment with atenolol (5 to 10 mg intravenously followed by 25 to 50 mg orally every 12 h), 98 to alinidine (20 to 40 mg intravenously followed by 20 to 40 mg orally every 8 h) and 94 to placebo. All patients received 100 mg of alteplase over 3 h and full intravenous heparinization. No significant differences in coronary artery patency, global ejection fraction or regional wall motion were observed at 10 to 14 days the three groups. Likewise, enzymatic and scintigraphic infarct size were also very similar. Neither atenolol nor alinidine was associated with a significant reduction in the incidence of arrhythmias during the 1st 24 h. No significant differences in clinical events were observed, with the exception of a greater incidence of nonfatal pulmonary edema in the atenolol group (6% vs. 1% in the alinidine group and 0% in the placebo group, p = 0.021).
Conclusions. In the absence of contraindications, the administration of a beta-blocker or a speciic bradycardiac agent together with thrombolytic therapy was safe. In this limited number of patients, these agents did not appear to enhance myocardiai salvage or preservation of left ventricular function or to reduce the incidence of major arrhythmias in the early phase of infarction.
☆ This study was supported by the Belgian National Fund for Scientific Research, ICI Pharma, Belgium and Boehringer Ingelheim, Belgium. It was presented in part at the 64th Annual Scientific Sessions of the American Heart Association, Anaheim, California, November 1991.
- Received May 22, 1992.
- Revision received December 21, 1992.
- Accepted February 9, 1993.