Biomedical subjects
Publications and source records attributed to John D Rutherford.
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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 2231 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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To identify electrocardiographic predictors of left ventricular enlargement or persistent dysfunction following a myocardial infarction. Baseline and predischarge 12-lead electrocardiograms (ECGs) from 272 patients with anterior myocardial infarction who were enrolled in the Healing and Early Afterload Reducing Therapy trial were evaluated and related to echocardiographic data obtained at baseline and day 90. ST-segment elevation, QRS score, and number of negative T waves were assessed at both time points. The majority of patients (87%; n = 237) received reperfusion therapy. Multivariate models were used to adjust for potential confounders, including maximal creatine kinase level and ejection fraction at baseline. None of the baseline electrocardiographic variables independently predicted ventricular enlargement or recovery of function. In contrast, the sum of ST- and maximum ST-segment elevation, and the number of leads with ST-segment elevation > or =1 mm in the predischarge ECG, were independent predictors of ventricular enlargement from baseline to day 90. Each lead with ST-segment elevation > or =1 mm was associated with 3.5 mL of ventricular enlargement (95% confidence interval [CI]: 1.6 to 5.5 mL; P <0.0001). Similarly, the sum of ST-segment elevation (odds ratio [OR] = 0.78; 95% CI: 0.69 to 0.89; P <0.0001), the maximum ST-segment elevation (OR = 0.25; 95% CI: 0.13 to 0.45; P <0.0001), and the number of leads with ST-segment elevation > or =1 mm (OR = 0.58; 95% CI: 0.45 to 0.74; P <0.0001) were independently associated with a lower likelihood of recovery of function at day 90. Predischarge ECG may be a useful tool for early identification of patients at risk of ventricular enlargement and persistent dysfunction following myocardial infarction.
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