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J Am Coll Cardiol, 2004; 43:2015-2021, doi:10.1016/j.jacc.2004.01.042 © 2004 by the American College of Cardiology Foundation |



* Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
University of Texas School of Public Health, Houston, Texas, USA
Department of Medicine, Brigham and Women's Hospital, and Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), Boston VA Healthcare System, Boston, Massachusetts, USA
University of Texas, Southwestern, Dallas, Texas, USA
|| Howard University Hospital, Washington, DC, USA
¶ Washington University School of Medicine, St. Louis, Missouri, USA
# Mount Sinai Medical Center, Miami, Florida, USA
** University of Montreal, Montreal, Canada
Manuscript received August 27, 2003; revised manuscript received December 17, 2003, accepted January 13, 2004.
* Reprint requests and correspondence: Dr. David Aguilar, University of Texas Health Science Center-Houston, Division of Cardiology, 6431 Fannin, MSB 1.246, Houston, Texas 77030, USA.
david.aguilar{at}uth.tmc.edu
OBJECTIVES: We assessed the influence of alcohol intake on the development of symptomatic heart failure (HF) in patients with left ventricular (LV) dysfunction after a myocardial infarction (MI).
BACKGROUND: In contrast to protection from coronary heart disease, alcohol consumption has been linked to cardiodepressant effects and has been considered contraindicated in patients with HF.
METHODS: The Survival And Ventricular Enlargement (SAVE) trial randomized 2,231 patients with a LV ejection fraction (EF) <40% following MI to an angiotensin-converting enzyme inhibitor or placebo. Patients were classified as nondrinkers, light-to-moderate drinkers (1 to 10 drinks/week), or heavy drinkers (>10 drinks/week) based on alcohol consumption reported at baseline. The primary outcome was hospitalization for HF or need for an open-label angiotensin-converting enzyme inhibitor. Analyses were repeated using alcohol consumption reported three months after MI.
RESULTS: Nondrinkers were older and had more comorbidities than light-to-moderate and heavy drinkers. In univariate analyses, baseline light-to-moderate alcohol intake was associated with a lower incidence of HF compared with nondrinkers (hazard ratio [HR] 0.71; 95% confidence interval [CI] 0.57 to 0.87), whereas heavy drinking was not (HR 0.91; 95% CI 0.67 to 1.23). After adjustment for baseline differences, light-to-moderate baseline alcohol consumption no longer significantly influenced the development of HF (light-to-moderate drinkers HR 0.93; 95% CI 0.75 to 1.17; heavy drinkers HR 1.25; 95% CI 0.91 to 1.72). Alcohol consumption reported three months after the MI similarly did not modify the risk of adverse outcome.
CONCLUSIONS: In patients with LV dysfunction after an MI, light-to-moderate alcohol intake either at baseline or following MI did not alter the risk for the development of HF requiring hospitalization or an open-label angiotensin-converting enzyme inhibitor.
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