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CLINICAL STUDIES

Light-to-moderate alcohol consumption and prognosis in patients with left ventricular systolic dysfunction

Howard A. Cooper, MD^* , Derek V. Exner, MD, MPH^* and Michael J. Domanski, MD, FACC^*

^* Clinical Trials Research Group, National Heart, Lung, and Blood Institute, Bethesda, Maryland, USA
Division of Cardiology, Georgetown University Medical Center, Washington, D.C., USA

Manuscript received September 14, 1999; revised manuscript received December 13, 1999, accepted February 9, 2000.

Reprint requests and correspondence: Dr. Howard A. Cooper, Two Rockledge Centre, Room 8149, 6701 Rockledge Drive, MSC 7936, Bethesda, Maryland 20892
Cooperh{at}nih.gov

	Abstract

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OBJECTIVES

The study evaluated the relationship between light-to-moderate alcohol consumption and prognosis in patients with left ventricular (LV) systolic dysfunction.

BACKGROUND

Although chronic consumption of large amounts of alcohol can lead to cardiomyopathy, the effects of light-to-moderate alcohol consumption in patients with LV dysfunction are unknown.

METHODS

The relationship between light-to-moderate alcohol consumption and prognosis was assessed in participants in the Studies of Left Ventricular Dysfunction (SOLVD), all of whom had ejection fraction values 0.35. Baseline characteristics and event rates of patients who consumed 1 to 14 drinks per week (light-to-moderate drinkers, n = 2,594) were compared with those of patients who reported no alcohol consumption (nondrinkers, n = 3,719). The association between light-to-moderate alcohol consumption and prognosis was evaluated using Cox proportional hazards analysis, controlling for baseline differences and important covariates.

RESULTS

Mortality rates were lower among light-to-moderate drinkers than among nondrinkers (7.2 vs. 9.4 deaths/100 person-years, p < 0.001). Among patients with ischemic LV dysfunction, light-to-moderate alcohol consumption was independently associated with a reduced risk of all-cause mortality (RR [relative risk] 0.85, p = 0.01), particularly for death from myocardial infarction (RR 0.55, p < 0.001). The risks of cardiovascular death, death from progressive heart failure, arrhythmic death, and hospitalization for heart failure were similar for light-to-moderate drinkers and nondrinkers in this group. Among patients with nonischemic LV dysfunction, light-to-moderate alcohol consumption had no significant effect on mortality (RR 0.93, p = 0.5).

CONCLUSIONS

Light-to-moderate alcohol consumption is not associated with an adverse prognosis in patients with LV systolic dysfunction, and it may reduce the risk of fatal myocardial infarction in patients with ischemic LV dysfunction.

Abbreviations and Acronyms   CI = confidence interval   EF = ejection fraction   HDL = high density lipoprotein   LV = left ventricular   MI = myocardial infarction   NYHA = New York Heart Association   RR = relative risk   SOLVD = Studies of Left Ventricular Dysfunction

	Methods

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The SOLVD Prevention and Treatment trials were randomized controlled studies that evaluated the efficacy of the angiotensin-converting-enzyme inhibitor enalapril in patients with LV systolic dysfunction. Patients 21 to 80 years of age with no history of intolerance to enalapril and an LV ejection fraction (EF) 0.35 were eligible for enrollment. Those with a recent myocardial infarction (MI), significant valvular heart disease, or other serious comorbid illness were excluded. Patients with chronic alcoholism were excluded only if this was deemed likely to interfere with patient compliance. Patients were required to be clinically stable and to have had no recent changes in their heart failure medications. The specific inclusion and exclusion criteria have been published (9–11). The SOLVD protocols were approved by the local institutional review board at each participating center and by the National Heart, Lung, and Blood Institute. Each participant provided written informed consent.

Collection of data.   All SOLVD participants (n = 6,797) underwent a detailed evaluation at entry. Patients were classified as asymptomatic or symptomatic and then enrolled in the Prevention or Treatment trial, respectively. There were 4,228 patients in the Prevention trial, approximately one third of whom had New York Heart Association (NYHA) functional class II symptoms. The Treatment trial included 2,569 patients, the majority of whom had NYHA functional class II and III symptoms.

At baseline, participants were asked the average number of alcoholic drinks they had consumed per week during the previous two years. Our analyses are based on these self-reported figures. Data on alcohol consumption were missing for 91 patients (1.3%), and these patients were excluded from this analysis. In addition, 97 patients (1.4%) who were diagnosed with alcoholic cardiomyopathy were excluded (Fig. 1).

View larger version (26K): [in this window] [in a new window]   Figure 1 Number of alcoholic drinks consumed per week at baseline for eligible participants in the Studies of Left Ventricular Dysfunction. (Percentages do not equal 100 because of rounding.)

Baseline variables.   Age, blood pressure, and LV EF values were assessed as continuous variables. All remaining variables, including study drug allocation (enalapril/placebo), were assessed as dichotomous variables. The NYHA functional class symptoms were grouped as class I, class II, or class III/IV. The etiology of LV systolic dysfunction was classified as ischemic or other (nonischemic) by the enrolling physician. Data on blood lipids were not collected.

Categorization of alcohol consumption.   To provide clinically meaningful information, patients were classified as nondrinkers (average consumption of zero alcoholic drinks per week), light-to-moderate drinkers (between 1 and 14 drinks per week), and heavy drinkers (more than 14 drinks per week).

Statistical analysis.   Data from the Prevention and Treatment trials were pooled after no interaction was found between trial assignment and alcohol consumption with regard to mortality. Evidence of statistical interaction between alcohol consumption and the etiology of LV dysfunction was observed (p = 0.05); thus, ischemic and nonischemic patients were separately evaluated. Continuous characteristics are presented as mean ± SD. Pairwise differences were evaluated using a chi-square test or t-test. Death from any cause was used as the primary end point in this analysis, and additional analyses were performed for cause-specific mortality end points and hospitalization for heart failure. Incidence rates were calculated as the number of events per 100 person-years of follow-up.

Multivariate Cox proportional hazards models were used to assess the independent relationship between alcohol consumption and mortality. Three multivariate models of increasing complexity were used in an attempt to highlight any confounding influences and to minimize the impact of missing data. The basic model included age, gender, EF, and NYHA class, adjusting for important demographic and prognostic factors. As the SOLVD trials were designed to assess the effect of enalapril, study drug assignment was also included in this model. An intermediate model added race, current smoking status, a history of diabetes and a history of hypertension, as these have also been shown to affect outcome and were likely to differ between drinkers and nondrinkers. Finally, a fully adjusted model, which also included the baseline use of digoxin, diuretics, beta-blockers, antiarrhythmic drugs, aspirin and anticoagulants, was used to assess for the possible confounding impact of baseline medication use. Relative risk (RR) estimates and 95% confidence intervals (CI) were obtained from the Cox models. Two-sided p values <0.05 were considered to be significant. All analyses were performed using Stata: Release 6.0 (College Station, Texas).

	Results

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Baseline characteristics.   The distribution of alcohol consumption at baseline for the 6,609 participants in SOLVD without alcoholic cardiomyopathy is displayed in Figure 1. Alcohol consumption ranged from 0 to 84 alcoholic drinks per week. The majority of participants (55%) were nondrinkers, while a substantial minority were light-to-moderate drinkers (38%) consuming 1 to 14 drinks per week. There were few heavy drinkers (6%) consuming >14 drinks per week. Because the small number of heavy drinkers precluded accurate risk estimates, this group was not analyzed further.

Baseline characteristics of nondrinkers and light-to-moderate drinkers are shown in Table 1. Differences in mean age, the proportion of women and minorities, NYHA class, the prevalence of diabetes and hypertension, and baseline medication use were observed. Mean EF was nearly identical in the two groups, and a similar proportion of both groups had ischemic cardiomyopathy. As anticipated, the proportion of participants who were current smokers was somewhat higher among light-to-moderate drinkers than among nondrinkers.

Multivariate analyses.   The results for participants with ischemic LV dysfunction (n = 5,331) and nonischemic LV dysfunction (n = 1,278) are presented in Table 3 and Table 4.

Nonischemic LV dysfunction (Table 4 ).   Light-to-moderate alcohol consumption, compared with no alcohol consumption, was not significantly associated with the risk of all-cause mortality or cardiovascular mortality in any of the models. The addition of markers of socioeconomic status to the models had little effect on the risk estimates (data not shown). A trend toward an increased risk of hospitalization for heart failure wasseen in patients with nonischemic cardiomyopathy (p = 0.1).

Cause-specific mortality end points (Table 5 ).  

In the SOLVD studies, only 22 deaths (1.5% of all deaths) were from violent causes. Eighteen patients died as a result of trauma, and four patients died as a result of suicide. The proportion of deaths from violent causes was similar between light-to-moderate drinkers (1.3%) and nondrinkers (1.5%).

	Discussion

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To our knowledge, this is the first analysis of the association between alcohol consumption and prognosis in a large cohort of patients with preexisting LV systolic dysfunction. Our data indicate that in patients with ischemic LV dysfunction, light-to-moderate alcohol consumption (1 to 14 alcoholic drinks/week) was associated with a modest reduction in the risk of death when compared with no alcohol consumption. Furthermore, light-to-moderate alcohol consumption was associated with a substantially reduced risk of fatal MI in this cohort. Heart failure progression, as indicated by either death from progressive heart failure or hospitalization for heart failure, was not associated with light-to-moderate alcohol consumption in patients with ischemic LV dysfunction. Among patients with nonischemic LV dysfunction, light-to-moderate alcohol consumption was not associated with an altered risk of all-cause mortality or death from any specific cause, including death from progressive heart failure. However, a trend toward an increased risk of hospitalization for heart failure was observed in this group.

Alcohol and coronary heart disease.   Most observational studies have demonstrated that light-to-moderate alcohol consumption is associated with a reduced risk of coronary heart disease (4–7). Coronary heart disease is the leading cause of systolic heart failure in the U.S., and it is an important cause of death and disease progression in this population (8). Thus, it is plausible that light-to-moderate alcohol consumption might have beneficial effects in patients with ischemic LV dysfunction. In SOLVD participants with ischemic LV dysfunction, light-to-moderate alcohol consumption was associated with a small but statistically significant reduction in all-cause mortality and a prominent reduction in the risk of fatal MI. A neutral association between light-to-moderate alcohol consumption and mortality was observed in patients with nonischemic LV dysfunction.

Alcohol and LV performance.   Previous research has demonstrated that heavy alcohol consumption is related to the development of cardiomyopathy. In animal models, chronic alcohol consumption leads to interstitial fibrosis and reduced myocardial contractility (1,12). In humans, chronic alcoholism is associated with a high prevalence of subclinical LV systolic dysfunction and histologic changes of cardiomyopathy (2). Despite this, there is no experimental evidence that light-to-moderate alcohol has a deleterious effect on LV performance. Indeed, invasive hemodynamic studies have generally demonstrated either no acute effect or a transient increase in LV contractility after the administration of a moderate amount of alcohol to patients with LV systolic dysfunction (13,14) or hypertrophic cardiomyopathy (15), or to normal volunteers (16,17). In the current analysis, no association between light-to-moderate alcohol consumption and the risk of heart failure progression (death from progressive heart failure or hospitalization for heart failure) was present in patients with ischemic LV dysfunction. Among those with nonischemic LV dysfunction, although a modest trend toward an increased risk of hospitalization for heart failure was seen, there was no increase in the risk of death from progressive heart failure. Taken together, these results suggest that light-to-moderate alcohol consumption does not significantly worsen preexisting LV dysfunction over the intermediate term.

Comparison to previous studies.   Our results agree closely with previous research. In a substudy of the Physicians’ Health Study, which examined the relationship between alcohol consumption and mortality in men following a first MI, consumption of one drink per day was associated with a RR reduction of 21% for all-cause mortality and 17% for cardiovascular mortality (18). These figures are similar to the RR reductions of 15% and 10% found in the current analysis for light-to-moderate drinkers with ischemic LV dysfunction.

Light-to-moderate alcohol consumption was associated with a prominent (45%) reduction in the risk of fatal MI in SOLVD participants with ischemic LV dysfunction. This reduction is similar in magnitude to that observed in the complete Physicians’ Health Study cohort, in which consumption of one drink per day was associated with a 35% RR reduction for a first MI (7). A case control study of a cohort of Kaiser Permanente patients found a RR reduction of 30% for MI in those who consumed 2 drinks daily when compared with nondrinkers. A smaller but still statistically significant risk reduction was seen even in the category of patients who consumed alcohol only infrequently (>1 drink per month but <1 drink per day) (19). The lack of association between light-to-moderate alcohol consumption and fatal myocardial infarction among SOLVD participants with nonischemic LV dysfunction is not surprising considering the rarity of this event.

Heavy alcohol consumption has been linked to cardiac arrhythmias, particularly atrial fibrillation but also ventricular arrhythmias (1,20). However, in our analysis, light-to-moderate alcohol consumption was associated with trends toward reductions in the risk of arrhythmic death among patients with either ischemic LV dysfunction or nonischemic LV dysfunction. These findings agree closely with previous studies. In the Kaiser Permanente study cohort, a comparable level of alcohol consumption was associated with a 20% reduction in the risk of sudden cardiac death (21), and in a population-based study from Washington State, the risk for primary cardiac arrest was 30% lower in light drinkers (>1 drink per month and <1 drink per day) compared with nondrinkers (22).

In the present analysis, light-to-moderate alcohol consumption was associated with a prominent reduction in the risk of noncardiovascular death among SOLVD participants with ischemic LV dysfunction. However, because the number of noncardiovascular deaths were few, these results should be interpreted with caution. Nonetheless, our findings are similar to those from the cohort of patients in the Physicians’ Health Study following a first MI, in whom one drink per day was associated with a 34% relative reduction in the risk of noncardiovascular death (18). Other studies have described a similar relationship (19,23,24). It has been postulated that noncardiovascular mortality may be lower because cardiovascular comorbidity is reduced in light-to-moderate drinkers (23,24). Further research is required to clarify this issue.

Study limitations.   Our analysis has several limitations. First, the relationship between alcohol consumption and prognosis may have been confounded by factors other than those for which we adjusted. This issue might be of particular importance in the analyses of cause-specific mortality end points, for which only the basic model was used. However, the detailed characterization of the SOLVD cohort, the small changes in risk estimates despite increasingly comprehensive statistical models, and the close agreement between our results and previous research make this less likely.

Second, our analyses are based on participants’ self-reported alcohol consumption. Although self-reported mild-to-moderate alcohol consumption is generally reliable, heavy drinkers tend to underreport their alcohol use (25). We attempted to minimize the effect of this possible underreporting by excluding participants with alcoholic cardiomyopathy; but even if a substantial number of heavy drinkers were incorrectly included with the light-to-moderate drinkers, our results would overestimate, rather than underestimate, any harmful effect of alcohol consumption.

Third, patients may have altered their drinking habits after entering the trial, an occurrence for which we could not adjust. Fourth, research in other patient populations has demonstrated that approximately 50% of the benefit of alcohol consumption with regard to coronary heart disease is brought about by its effects on high density lipoprotein (HDL) cholesterol levels (4). Because blood lipid values were not collected in the SOLVD trials, we were unable to analyze this relationship. Finally, the average duration of follow-up in SOLVD was only about three years. Therefore, we lack information on the long-term effects of alcohol consumption in this population.

Conclusions.   Light-to-moderate alcohol consumption appears to be safe in patients with LV systolic dysfunction, and it may reduce the risk of death and the risk of fatal MI in patients with ischemic LV dysfunction. Patients with LV dysfunction who consume 2 drinks per day should not be advised to discontinue drinking alcohol for the purpose of reducing cardiovascular morbidity or mortality. However, there is insufficient evidence to recommend the use of alcohol to patients with LV dysfunction who do not currently drink alcohol. Heavy alcohol consumption should continue to be discouraged for patients with LV systolic dysfunction, because of the clear increase in noncardiovascular and total mortality shown in previous studies (19,23,24) and because of the strong evidence that heavy alcohol consumption can lead to impairment of LV contractile function (1,2,12).

	Footnotes

 
Dr. Cooper is supported by an intramural research training award from the National Institutes of Health. Dr. Exner is supported by the Medical Research Council of Canada and the Alberta Heritage Foundation for Medical Research.

	References

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1. Regan TJ, Haider B. Ethanol abuse and heart disease. Circulation 1981;64 Suppl III:III-14–9.
2. Urbano-Marquez A, Estruch R, Navarro-Lopez F, Grau JM, Mont L, Rubin E. The effects of alcoholism on skeletal and cardiac muscle. N Engl J Med. 1989;321:1048–1050[Medline]
3. Williams JF, Bristow MR, Fowler MB, et al. Guidelines for the evaluation and management of heart failure. Report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Evaluation and Management of Heart Failure). Circulation. 1995;92:2764–2784[Free Full Text]
4. Pearson TA. Alcohol and heart disease. AHA Scientific Statement. Circulation. 1996;94:3023–3025[Free Full Text]
5. Moore RD, Pearson TA. Moderate alcohol consumption and coronary artery disease: a review. Medicine. 1986;65:242–267[Medline]
6. Klatsky AL, Armstrong MA, Friedman GD. Risk of cardiovascular mortality in alcohol drinkers, ex-drinkers, and nondrinkers. Am J Cardiol. 1990;66:1237–1242[CrossRef][Medline]
7. Camargo CA, Stampfer MJ, Glynn RJ, et al. Moderate alcohol consumption and risk for angina pectoris or myocardial infarction in U.S. male physicians. Ann Intern Med. 1997;126:372–375[Abstract/Free Full Text]
8. Bourassa MG, Gurne O, Bangdiwala SI, et al. Natural history and patterns of current practice in heart failure. J Am Coll Cardiol 1993;22 Suppl A:14A–9.
9. SOLVD Investigators. Effect of enalapril on mortality and the development of heart failure in asymptomatic patients with reduced left ventricular ejection fractions. N Engl J Med. 1992;327:685–691[Abstract]
10. SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med. 1991;325:293–302[Abstract]
11. SOLVD Investigators. Studies of Left Ventricular Dysfunction (SOLVD)—rationale, design, and methods: two trials that evaluate the effect of enalapril in patients with reduced ejection fraction. Am J Cardiol. 1990;66:315–322[CrossRef][Medline]
12. Sanderson JE, Jones JV, Graham DI. Effect of chronic alcohol ingestion on the heart and blood pressure of spontaneously hypertensive rats. Clin Exp Hypertens. 1983;A5:673–689
13. Greenberg BH, Schultz R, Grunkemeier GL, Griswold H. Acute effects of alcohol in patients with congestive heart failure. Ann Intern Med. 1982;97:171–175[Medline]
14. Kelbaek H, Heslet L, Skagen K, Munck O, Christensen NJ, Godtfredsen J. Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study. Alcohol Alcohol. 1988;23:17–21[Abstract/Free Full Text]
15. Paz R, Jortner R, Tunick PA, et al. The effect of the ingestion of ethanol on obstruction of the left ventricular outflow tract in hypertrophic cardiomyopathy. N Engl J Med. 1996;335:938–941[Abstract/Free Full Text]
16. Juchems R, Klobe R. Hemodynamic effects of ethyl alcohol in man. Am Heart J. 1969;78:133–135[CrossRef][Medline]
17. Gould L, Jaynal F, Zahir M, Gomprecht RF. Effects of alcohol on the systolic time intervals. Q J Stud Alcohol. 1972;33:451–463[Medline]
18. Muntwyler J, Hennekens CH, Buring JE, Gaziano JM. Mortality and light to moderate alcohol consumption after myocardial infarction. Lancet. 1998;352:1882–1885[CrossRef][Medline]
19. Klatsky AL, Armstrong MA, Friedman GD. Alcohol and mortality. Ann Intern Med. 1992;117:646–654[CrossRef][Medline]
20. Kupari M, Koskinen P. Alcohol, cardiac arrhythmias and sudden death. Novartis Found Symp. 1998;216:68–79[Medline]
21. Klatsky AL, Friedman GD, Siegelaub AB. Alcohol use, myocardial infarction, sudden cardiac death, and hypertension. Alcohol Clin Exp Res. 1979;3:33–39[Medline]
22. Siscovick DS, Weiss NS, Fox N. Moderate alcohol consumption and primary cardiac arrest. Am J Epidemiol. 1986;123:499–503[Abstract/Free Full Text]
23. Thun JT, Peto R, Lopez AD, et al. Alcohol consumption and mortality among middle-aged and elderly US adults. N Engl J Med. 1997;337:1705–1714[Abstract/Free Full Text]
24. Doll R, Peto R, Hal E, Wheatley K, Gray R. Mortality in relation to consumption of alcohol: 13 years’ observations on male British doctors. BMJ. 1994;309:911–918[Abstract/Free Full Text]
25. Cahalan D. Quantifying alcohol consumption: patterns and problems. Circulation. 1981;64(Suppl III):III-7–III-14

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