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J Am Coll Cardiol, 1998; 32:634-640 © 1998 by the American College of Cardiology Foundation |
a Division of Cardiology, University Hospital Basel, Basel, Switzerland
* Institute for Clinical Evaluative Sciences, North York, Ontario, Canada
Duke Clinical Research Institute, Durham, North Carolina, USA
Cleveland Clinic Foundation, Cleveland, Ohio, USA
University Hospital Gasthuisberg, Leuven, Belgium
|| Department of Medicine, University of Alberta, Edmonton, Canada
Manuscript received February 10, 1998; revised manuscript received May 5, 1998, accepted May 20, 1998.
Address for correspondence: Dr. Christopher B. Granger, Duke Clinical Research Institute, 2024 West Main Street, Bay A-1, Durham, North Carolina 27705
grang001{at}mc.duke.edu
Objectives. We assessed the use and effects of acute intravenous and later oral atenolol treatment in a prospectively planned post hoc analysis of the GUSTO-I dataset.
Background. Early intravenous beta blockade is generally recommended after myocardial infarction, especially for patients with tachycardia and/or hypertension and those without heart failure.
Methods. Besides one of four thrombolytic strategies, patients without hypotension, bradycardia or signs of heart failure were to receive atenolol 5 mg intravenously as soon as possible, another 5 mg intravenously 10 min later and 50 to 100 mg orally daily during hospitalization. We compared the 30-day mortality of patients given no atenolol (n = 10,073), any atenolol (n = 30,771), any intravenous atenolol (n = 18,200), only oral atenolol (n = 12,545) and both intravenous and oral drug (n = 16,406), after controlling for baseline differences and for early deaths (before oral atenolol could be given).
Results. Patients given any atenolol had a lower baseline risk than those not given atenolol. Adjusted 30-day mortality was significantly lower in atenolol-treated patients, but patients treated with intravenous and oral atenolol treatment vs. oral treatment alone were more likely to die (odds ratio, 1.3; 95% confidence interval, 1.0 to 1.5; p = 0.02). Subgroups had similar rates of stroke, intracranial hemorrhage and reinfarction, but intravenous atenolol use was associated with more heart failure, shock, recurrent ischemia and pacemaker use than oral atenolol use.
Conclusions. Although atenolol appears to improve outcomes after thrombolysis for myocardial infarction, early intravenous atenolol seems of limited value. The best approach for most patients may be to begin oral atenolol once stable.
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