Abstract/Text
AIMS: The outcome of alcoholic cardiomyopathy is thought to be better than idiopathic dilated cardiomyopathy if patients abstain from alcohol. The aim of this study was to compare the long-term clinical outcome of alcoholic and idiopathic dilated cardiomyopathy.
METHODS AND RESULTS: Of 134 patients with dilated cardiomyopathy and normal coronary angiography, 50 had alcoholic cardiomyopathy; they were compared serially to 84 patients with idiopathic dilated cardiomyopathy. Left ventricular end-diastolic diameter, left ventricular ejection fraction and cardiac index, severity of ventricular arrhythmias, measurement of heart rate variability and results of signal-averaged ECG were similar in both groups. Although alcohol withdrawal was strongly recommended but observed in only 70% of patients with alcoholic cardiomyopathy, both groups had similar outcome in terms of cardiac death after follow-up treatment of 47+/-40 months. Multivariate analysis in the entire cohort demonstrated that increased pulmonary capillary wedge pressure (P=0. 003), alcoholism and lack of abstinence during follow-up (P=0.006) and decreased standard deviation of all normal-to-normal RR intervals (P=0.02) were independent predictors of cardiac death.
CONCLUSION: In contrast with previous studies, patients with alcoholic cardiomyopathy did not have a better outcome than patients with idiopathic dilated cardiomyopathy. Alcoholism without abstinence was a strong predictor of cardiac death. This suggests that a more aggressive approach to alcohol cessation is needed in these patients.
Copyright 2000 The European Society of Cardiology.
Abstract/Text
BACKGROUND: Alcohol has been implicated as a risk factor for idiopathic dilated cardiomyopathy (DCM), but a causal relation has not been established. The objective of this study was to determine the association between alcohol consumption and DCM.
METHODS: Questionnaires detailing average weekly intake of alcohol, total lifetime consumption, and alcohol abuse were administered in a cohort of well-defined patients with DCM and a randomly selected, population-based control group.
RESULTS: Significantly more of the 100 patients with DCM than the 211 members of the control group drank greater than the recommended weekly intake of alcohol (40% vs 24%; p < 0.01) and were alcohol abusers according to the CAGE questionnaire (27% vs 16%; p < 0.05). The average total lifetime consumption measured in units of alcohol was also significantly greater in cases than in the control group (31,200 vs 7,904; p < 0.01). Patients with familial DCM were not significantly more likely to consume alcohol above recommended limits or to be alcohol abusers compared with nonfamilial cases.
CONCLUSIONS: This study confirms previous suspicion of a causal association between alcohol and DCM, with significantly more patients than members of the control group either abusing alcohol or drinking it in excess of recommended limits.
Abstract/Text
Systolic left ventricular dysfunction is relatively common in even asymptomatic alcoholics, but whether diastolic function is also altered is much less well-studied. We used M-mode and Doppler echocardiography to study left ventricular size, mass, systolic function and diastolic filling in 32 alcoholics free of clinically detectable heart disease and in 15 healthy control subjects. Left ventricular mass index and posterior wall thickness were higher in alcoholics than in controls, but there was no statistically significant difference either in end-diastolic size or in systolic ventricular function. More abnormalities were found in the Doppler indexes of diastolic function, however. The alcoholics had a prolonged relaxation time (200 +/- 6 vs 184 +/- 5 ms [mean +/- standard error], p less than 0.05), a decreased peak early diastolic velocity (52 +/- 2 vs 60 +/- 3 cm/s, p less than 0.05), a slower acceleration of the early flow (410 +/- 18 vs 552 +/- 43 cm/s2, p less than 0.01), and a higher atrial-to-early peak velocity ratio (0.74 +/- 0.04 vs 0.60 +/- 0.05, p less than 0.05). This pattern of changes suggests a primary abnormality in the relaxation of the left ventricle. In multivariate analyses, the abnormalities in the Doppler indexes were independent of the duration of alcoholism, the quantity of the most recent ethanol exposure and the increased mass of the left ventricle. Impaired early filling of the left ventricle due to delayed relaxation is common in asymptomatic alcoholics and may in fact be the earliest functional sign of preclinical alcoholic cardiomyopathy.
Abstract/Text
OBJECTIVES: This study sought to assess preclinical cardiac abnormalities in chronic alcoholic patients and possible differences among alcoholics related to the duration of heavy drinking.
BACKGROUND: Chronic excessive alcohol intake has been reported as a possible cause of dilated cardiomyopathy. However, before the appearance of severe cardiac dysfunction, subtle signs of cardiac abnormalities may be identified.
METHODS: We studied 30 healthy subjects (age 44 +/- 8 years) and 89 asymptomatic alcoholics (age 45 +/- 8 years, p = NS) divided into three groups, with short (S, 5-9 years, n = 31), intermediate (I, 10-15 years, n = 31) and long (L, 16-28 years, n = 27) duration of alcoholism. Transmitral early (E) and late (A) Doppler flow velocities, E/A ratio, deceleration time of E (DT) and isovolumic relaxation time (IVRT) were obtained. Left ventricular (LV) wall thickness and volumes were also determined by echocardiography, and LV mass and ejection fraction (EF) were calculated.
RESULTS: The alcoholics had prolonged IVRT (92 +/- 11 vs. 83 +/- 7 ms, p < 0.001), longer DT (180 +/- 20 vs. 170 +/- 10 ms, p < 0.01), smaller E/A (1.25 +/- 0.34 vs. 1.40 +/- 0.32, p < 0.05), larger LV volumes (73 +/- 8 vs. 65 +/- 7 ml/m2, p < 0.001 for end-diastolic volume index; 25 +/- 4 vs. 21 +/- 2 ml/m2, p < 0.001 for end-systolic volume index), higher LV mass index (92 +/- 14 vs. 78 +/- 8 g/m2, p < 0.001) and thicker posterior wall (9 +/- 1 vs. 8 +/- 1 mm, p < 0.001). Ejection fraction did not differ between the two groups (66 +/- 4 vs. 67 +/- 2%). Deceleration time of the early transmitral flow velocity was longer in groups L (187 +/- 18 ms) and I (185 +/- 16 ms) compared with group S (168 +/- 17 ms, p < 0.001 for L and I vs. S), whereas A was higher in group L compared with S (43 +/- 10 vs. 51 +/- 10 cm/s, p < 0.005). Multiple regression analysis identified duration of heavy drinking as the most important variable affecting DT and A.
CONCLUSIONS: Left ventricular dilation with preserved EF and impaired LV relaxation characterized LV function in chronic asymptomatic alcoholic patients. It appeared that the progression of abnormalities in LV diastolic filling related to the duration of alcoholism.
Abstract/Text
The echocardiogram and systolic time intervals were used to evaluate cardiac function in 73 chronic alcoholic subjects without symptoms of heart disease. All were below the age of 45 years and none had arterial hypertension or history of heart disease. The echocardiograms of chronic alcoholic individuals revealed increased thickness of the left ventricular wall (10.4 mm. +/- 1.05, normal controls 8.76 mm. +/- .86, p less than 0.001), interventricular septum (11.71 mm. +/- 1.33, normal controls 9.63 +/- 1.24, p less than 0.001) and markedly increased left ventricular mass (145 gm./M.2 +/- 32, normal controls 101 +/- 20.7, p less than 0.001). The echocardiographic indices of myocardial contractility (ejection fraction, wall excursion and velocity, circumferential fiber shortening) were normal. Systolic time intervals revealed shortening of ejection time and prolongation of the pre-ejection period. It was found that approximately half of the asymptomatic alcoholic subjects have left ventricular hypertrophy without echocardiographic evidence of decreased myocardial contractility. It is suggested that abnormal systolic time intervals may be due to decreased myocardial compliance.
Abstract/Text
M-mode echo recordings of the left ventricle and left ventricular inflow Doppler velocimetry were performed in 34 male alcoholics below age 45 and in 25 nonalcoholic male controls. Groups were well matched for age, body surface area and heart rate. Systolic arterial pressure was slightly higher in alcoholics and none of the subjects studied had cardiorespiratory symptoms. Data from imaging echocardiography (M-mode echo) were comparable in both groups, and fractional shortening, reflecting left ventricular systolic performance, was identical. Left ventricular inflow Doppler velocimetry showed quite different results in alcoholics and control subjects for the early diastolic flow velocity peak (0.52 +/- 0.12 versus 0.61 +/- 0.11 m/s; p less than 0.01) and in peak flow velocities in the atrial contraction phase (0.32 +/- 0.11 versus 0.27 +/- 0.06 m/s; p less than 0.05). The lower ratio of both velocities in patients (1.88 +/- 0.95 versus 2.34 +/- 0.60 m/s; p less than 0.05) suggests that left ventricular distensibility is altered in alcoholics. In addition, isovolumetric relaxation period, reflecting an early diastolic event, was slightly but significantly prolonged in alcoholic subjects (68 +/- 14 versus 56 +/- 10 ms; p less than 0.001). It is concluded that diastolic performance is altered in young alcoholics without cardiorespiratory symptoms showing normal systolic performance, and that these alterations may be an early marker of alcoholic cardiomyopathy.
David Aguilar, Hicham Skali, Lemuel A Moyé, Eldrin F Lewis, J Michael Gaziano, John D Rutherford, L Howard Hartley, Otelio S Randall, Edward M Geltman, Gervasio A Lamas, Jean L Rouleau, Marc A Pfeffer, Scott D Solomon
Alcohol consumption and prognosis in patients with left ventricular systolic dysfunction after a myocardial infarction.
J Am Coll Cardiol. 2004 Jun 2;43(11):2015-21. doi: 10.1016/j.jacc.2004.01.042.
Abstract/Text
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.
Abstract/Text
CONTEXT: Heavy consumption of alcohol can lead to heart failure, but the relationship between moderate alcohol consumption and risk of heart failure is largely unknown.
OBJECTIVE: To determine whether moderate alcohol consumption predicts heart failure risk among older persons, independent of the association of moderate alcohol consumption with lower risk of myocardial infarction (MI).
DESIGN: Prospective cohort study conducted from 1982 through 1996, with a maximum follow-up of 14 years.
SETTING AND PARTICIPANTS: Population-based sample of 2235 noninstitutionalized elderly persons (mean age, 73.7 years; 41.2% male; 21.3% nonwhite) residing in New Haven, Conn, who were free of heart failure at baseline. Persons who reported alcohol consumption of more than 70 oz in the month prior to baseline were excluded.
MAIN OUTCOME MEASURE: Time to first fatal or nonfatal heart failure event, according to the amount of alcohol consumed in the month prior to baseline.
RESULTS: Increasing alcohol consumption in the moderate range was associated with decreasing heart failure rates. For persons consuming no alcohol (50.0%), 1 to 20 oz (40.2%), and 21 to 70 oz (9.8%) in the month prior to baseline, crude heart failure rates per 1000 years of follow-up were 16.1, 12.2, and 9.2, respectively. After adjustment for age, sex, race, education, angina, history of MI and diabetes, MI during follow-up, hypertension, pulse pressure, body mass index, and current smoking, the relative risks of heart failure for those consuming no alcohol, 1 to 20 oz, and 21 to 70 oz in the month prior to baseline were 1.00 (referent), 0.79 (95% confidence interval [CI], 0.60-1.02), and 0.53 (95% CI, 0.32-0.88) (P for trend =.02).
CONCLUSIONS: Increasing levels of moderate alcohol consumption are associated with a decreasing risk of heart failure among older persons. This association is independent of a number of confounding factors and does not appear to be entirely mediated by a reduction in MI risk.
Abstract/Text
OBJECTIVES: We investigated the association between alcohol consumption and incident congestive heart failure (CHF) both overall and after adjusting for incident myocardial infarction (MI).
BACKGROUND: Moderate alcohol consumption has been associated with lower risk of CHF and MI.
METHODS: The Cardiovascular Health study, a prospective cohort study of cardiovascular disease risk factors and outcomes, followed 5,888 subjects > or =65 years old for 7 to 10 years. Cox models were used to estimate the adjusted risk of CHF by reported alcohol consumption.
RESULTS: There were 5,595 subjects at baseline at risk for incident CHF with alcohol data and 1,056 events during follow-up. Compared with abstainers, the adjusted risk of CHF was lower among subjects who reported consuming 1 to 6 drinks per week (hazard ratio [HR] 0.82, 95% confidence interval [CI] 0.67 to 1.00, p = 0.05) and 7 to 13 drinks per week (HR 0.66, 95% CI 0.47 to 0.91, p = 0.01). Time-dependent adjustment for incident MI altered only slightly the association between moderate alcohol consumption and CHF (for 1 to 6 drinks per week, HR 0.84, 95% CI 0.65 to 1.04; for 7 to 13 drinks per week, HR 0.69, 95% CI 0.49 to 0.99). Baseline former drinkers had a higher risk of CHF than abstainers (HR 1.51, p < 0.01), but those who quit during the study did not have a higher risk (HR 0.83, 95% CI 0.66 to 1.03).
CONCLUSIONS: Moderate alcohol use is associated with a lower risk of incident CHF among older adults, even after accounting for incident MI and other factors.
Abstract/Text
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 < or = 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.
Abstract/Text
BACKGROUND: Although excessive alcohol consumption can promote cardiomyopathy, little is known about the association between alcohol consumption and risk for congestive heart failure in the community.
OBJECTIVE: To determine the relation between alcohol consumption and risk for congestive heart failure in the community.
DESIGN: Community-based, prospective observational study.
SETTING: Framingham, Massachusetts.
PARTICIPANTS: Participants in the Framingham Heart Study who were free of congestive heart failure and coronary heart disease.
MEASUREMENTS: Self-reported alcohol consumption; sex-specific rates of congestive heart failure per 1000 person-years of follow-up by level of alcohol consumption.
RESULTS: In men, 99 cases of congestive heart failure occurred during 26 035 person-years of follow-up. In women, 120 cases of congestive heart failure occurred during 35 563 person-years of follow-up. After adjustment for multiple confounders, risk for congestive heart failure was lower among men at all levels of alcohol consumption compared with men who consumed less than 1 drink/wk. The hazard ratio for congestive heart failure was lowest among men who consumed 8 to 14 drinks/wk (0.41 [95% CI, 0.21 to 0.81]) compared with those who consumed less than 1 drink/wk. In women, the age-adjusted hazard ratio for congestive heart failure was lowest among those who consumed 3 to 7 drinks/wk (0.49 [CI, 0.25 to 0.96]) compared with those who consumed less than 1 drink/wk. However, after adjustment for multiple predictors of congestive heart failure, this association was no longer statistically significant.
CONCLUSIONS: In the community, alcohol consumption is not associated with increased risk for congestive heart failure, even among heavy drinkers (> or = 15 drinks/wk in men and > or = 8 drinks/wk in women). To the contrary, when consumed in moderation, alcohol appears to protect against congestive heart failure.
Abstract/Text
Alcohol use, abuse, and dependence have the potential to result in alcoholic cardiomyopathy (ACM). This distinct form of congestive heart failure (CHF) is responsible for 21-36% of all cases of nonischemic dilated cardiomyopathy in Western society. Without complete abstinence, the 4-year mortality for ACM approaches 50%. Therefore, accurate and detailed assessment of alcohol use in congestive heart failure is essential. The prevalence of problematic alcohol use is unrecognized by many clinicians. Clinical assessment of alcohol intake is often reduced to a simple question such as, "Do you drink?" Denial and minimization are hallmarks of alcohol abuse, with many individuals underreporting their use of alcohol. Clinicians can overcome these hurdles by implementing practical history taking measures to improve the accuracy of self-reported alcohol use. The data regarding the dangers of ongoing alcohol use in individuals with ACM make attempts to engage individuals in treatment to support abstinence essential. Suggestions for detailed and accurate assessment are discussed.
Abstract/Text
Although a relationship has been suggested between abstinence from alcohol and improvement in left ventricular (LV) function, no long-term studies in large groups of patients have been done to confirm this impression or to demonstrate an effect on survival. To address these questions, the authors analyzed the outcome in 105 male patients with alcoholic cardiomyopathy and 64 control male patients with nonalcoholic dilated cardiomyopathy. Survival data were available for all patients. The correlates of survival were assessed via the Cox proportional hazards model. Variables considered were age, race, drinking pattern (current drinker versus former drinker), presence of coronary artery disease (CAD), hypertension, and diabetes, and these echo variables: left atrial (LA) size, posterior wall thickness, LV end diastolic dimension (LVDD), minimal E point septal separation, wall motion, presence of incomplete mitral leaflet closure (IMLC) or low cardiac output, and the ratio of relative wall thickness to LVDD. The two study groups were comparable with respect to all echocardiographic variables. At a mean follow-up of 17.2 months +/- 12.1 months, 42.85% of the alcoholics and 41% of the nonalcoholics had died. Nonsurvival in the alcoholic group was significantly associated with only two factors: an increased LVDD and the presence of IMLC. The drinking pattern was not significantly associated with survival. By contrast, in the nonalcoholics,the variables most closely related to survival were LVDD, low cardiac output, increasing age, and abnormal wall motion. Therefore: (1) the risk factors in alcoholic and nonalcoholic cardiomyopathy are similar although IMLC appears to be a relatively specific prognostic factor for alcoholic cardiomyopathy and (2) abstinence from alcohol does not appear to improve survival.
Abstract/Text
In patients with alcoholic cardiomyopathy there is evidence that mild heart failure is reversible if patients abstain from alcohol, but there is no consensus whether the disease is progressive once structural myocardial dilation has evolved. The aim of the present study was to compare the long-term course of congestive heart failure due to alcoholic and idiopathic dilated cardiomyopathy. Of 75 patients with overt congestive heart failure, 23 had alcoholic cardiomyopathy and were compared to 52 patients with idiopathic cardiomyopathy. The mean age was 48 +/- 12 years. Despite medical therapy, heart failure class New York Heart Association III-IV was present in 52% of patients with alcoholic and 47% of patients with idiopathic cardiomyopathy (not significant). Their mean left ventricular ejection fraction was 30 +/- 12% vs 28 +/- 12% and left ventricular end-diastolic volumes were 264 +/- 125 ml and 254 +/- 100 ml respectively (not significant). Overall survival at 1, 5 and 10 years was 100%, 81% and 81% for the group with alcoholic dilated cardiomyopathy and 89%, 48% and 30% for the group with idiopathic cardiomyopathy, respectively (P = 0.041), and the difference was even greater for transplant-free survival P = 0.005). Clinical and invasive signs of left and right heart failure as well as left ventricular dimensions were predictive of a fatal outcome; however, symptom duration and left ventricular volumes were only predictive in patients with idiopathic cardiomyopathy, suggesting that in the two patient groups different mechanisms may lead to death. Mortality in patients with severe congestive heart failure and left ventricular dilatation due to alcoholic cardiomyopathy is significantly lower than that in patients with idiopathic cardiomyopathy and similar degrees of heart failure. Thus, despite structural changes inherent in marked left ventricular dilatation, disease progression in alcoholic dilated cardiomyopathy is different from that in idiopathic cardiomyopathy and thus may have implications for the choice of therapy.
