Clinical Trajectories and Long-Term Outcomes of Alcoholic Versus Other Forms of Dilated Cardiomyopathy.

BACKGROUND: Alcoholic cardiomyopathy (ACM) is a form of dilated cardiomyopathy (DCM) occurring secondary to long-standing heavy alcohol use and is associated with poor outcomes, but the cause-specific risks are insufficiently understood. METHOD: Between 1997 and 2018, we identified all patients with a first diagnosis of ACM or DCM. The cumulative incidence of different causes of hospitalisation and mortality in the two groups was calculated using the Fine-Gray and Kaplan-Meier methods. RESULTS: A Total of 1,237 patients with ACM (mean age 56.3±10.1 years, 89% men) and 17,211 individuals with DCM (mean age 63.6±13.8 years, 71% men) were identified. Diabetes (10% vs 15%), hypertension (22% vs 31%), and stroke (8% vs 10%) were less common in ACM than DCM, whereas obstructive lung disease (15% vs 12%) and liver disease (17% vs 2%) were more prevalent (p<0.05). Cumulative 5-year mortality was 49% in ACM vs 33% in DCM, p<0.0001, multivariable adjusted hazards ratio 2.11 (95% confidence interval 1.97-2.26). The distribution of causes of death was similar in ACM and DCM, with the predominance of cardiovascular causes in both groups (42% in ACM vs 44% in DCM). 5-year cumulative incidence of heart failure hospitalisations (48% vs 54%) and any somatic cause (59% vs 65%) were also similar in ACM vs DCM. At 1 year, the use of beta blockers (55% vs 80%) and implantable cardioverter defibrillators (3% vs 14%) were significantly less often used in ACM vs DCM. CONCLUSIONS: Patients with ACM had similar cardiovascular risks and hospitalisation patterns as other forms of DCM, but lower use of guideline-directed cardiovascular therapies and greater mortality.

Contemporary Appraisal of Sex Differences in Prevalence, Correlates, and Outcomes of Alcoholic Cardiomyopathy.

AIMS: The aims of this study were to: examine differences in alcoholic cardiomyopathy (ACM) prevalence, temporal trends and the distribution of socio-demographic factors and comorbidities by sex; and investigate differences in selected inpatient outcomes between women and men with ACM. METHODS: We used the 2002-2014 Nationwide Inpatient Sample databases. Overall and sex-specific rates of ACM were estimated across sociodemographic, clinical, and hospital characteristics. Joinpoint regression was used to estimate temporal trends (annual percent change [APC]) of ACM-related hospitalization by sex and race/ethnicity. Adjusted odds ratios (AOR) representing associations between sex and selected ACM outcomes were calculated using survey logistic regression. RESULTS: The rate of ACM among all inpatient men and women was 128 per 100,000 and 17 per 100,000 hospitalizations, respectively. Among women, the rate of ACM remained unchanged during the study period, while for men, there was 1.2% annual reduction from 2002-2010 (APC -1.3, 95% CI: -1.7, -0.8). Women with ACM were more likely than men with ACM to experience depression (AOR=2.24, 95% CI: 2.06-2.43) and anxiety (AOR=1.94, 95% CI: 1.75-2.15), while men with ACM were 21% and 24% more likely than women with ACM to experience 'any heart failure (HF)' and HF with reduced ejection fraction respectively. One in 1,471 hospitalizations were related to ACM with a male-to-female ratio of 8:1. CONCLUSION: Individuals with ACM are at increased likelihood of adverse outcomes. Women with ACM are at increased risk of depression and anxiety, while men are at increased risk of HF.

Alcoholic cardiomyopathy: a review.

Alcohol abuse can cause cardiomyopathy indistinguishable from other types of dilated nonischemic cardiomyopathy. Most heavy drinkers remain asymptomatic in the earlier stages of disease progression, and many never develop the familiar clinical manifestations that typify heart failure. We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy. The relationship of alcohol to heart disease is complicated by the fact that in moderation, alcohol has been shown to afford a certain degree of protection against cardiovascular disease.

Cirrhotic cardiomyopathy.

The presence of cardiocirculatory dysfunction in liver cirrhosis has been described since 1960 and it was exclusively attributed to alcoholic cardiomyopathie. Only in the last two decades, the term of cirrhotic cardiomyopathy (CCM) was introduced to describe cardiac dysfunction in patients with cirrhosis. This entity is currently underdiagnosed because the disease is usually latent and manifests when the patient is under stress. However, overt cardiac failure has been described after transjugular intrahepatic portosystemic shun and liver transplantation. The diagnosis of CCM is still difficult to determine because of the lack of specific diagnosis tools. CCM is characterized by systolic dysfunction, diastolic dysfunction and electrophysiological abnormalities. At present, there is no specific treatment outside liver transplantation in the light of increased mortality and postoperative complications.Our review provides an overview of CCM, its definition, prevalence, pathogenic mechanisms, clinical presentation, various explorations and management in light of the most recent published literature.

Alcohol use disorders and the heart.

Alcohol use is an important preventable and modifiable cause of non-communicable disease, and has complex effects on the cardiovascular system that vary with dose. Observational and prospective studies have consistently shown a lower risk of cardiovascular and all-cause mortality in people with low levels of alcohol consumption when compared to abstainers (the 'J'-shaped curve). Maximum potential benefit occurs at 0.5 to one standard drinks (7-14 g pure ethanol) per day for women (18% lower all-cause mortality, 95% confidence interval (CI) = 13-22%) and one to two standard drinks (14-28 g ethanol) per day for men (17% lower all-cause mortality, 95% CI = 15-19%). However, this evidence is contested, and overall the detrimental effects of alcohol far outweigh the beneficial effects, with the risk of premature mortality increasing steadily after an average consumption of 10 g ethanol/day. Blood pressure (BP) is increased by regular alcohol consumption in a dose-dependent manner, with a relative risk for hypertension (systolic BP > 140 mm Hg or diastolic > 90 mm Hg) of 1.7 for 50 g ethanol/day and 2.5 at 100 g/day. Important reductions in BP readings can be expected after as little as 1 month of abstinence from alcohol. Heavy alcohol consumption in a binge pattern is associated with the development of acute cardiac arrhythmia, even in people with normal heart function. Atrial fibrillation is the most common arrhythmia associated with chronic high-volume alcohol intake, and above 14 g alcohol/day the relative risk increases 10% for every extra standard drink (14 g ethanol). Ethanol and its metabolites have toxic effects on cardiac myocytes, and alcoholic cardiomyopathy (ACM) accounts for a third of all cases of non-ischaemic dilated cardiomyopathy. Screening people drinking alcohol above low-volume levels and delivering a brief intervention may prevent the development of cardiovascular complications. Although people with established cardiovascular disease show improved outcomes with a reduction to low-volume alcohol consumption, there is no safe amount of alcohol to drink and patients with ACM should aim for abstinence in order to optimize medical treatment.

National trends in hospitalizations and outcomes in patients with alcoholic cardiomyopathy.

BACKGROUND: Numerous studies have shown conflicting results regarding the natural history and outcomes with alcoholic cardiomyopathy (AC). HYPOTHESIS: Determining the trends in hospitalization among patients with AC and associated outcomes will facilitate a better understanding of this disease. METHODS: We conducted our analysis on discharge data from the Healthcare Cost and Utilization Project-Nationwide Inpatient Sample (HCUP-NIS) from 2002 through 2014. We obtained data from patients aged ≥18 years with diagnosis of "Alcoholic Cardiomyopathy." Death was defined within the NIS as in-hospital mortality. By using International Classification of Disease-9th edition-Clinical Modification (ICD-9CM) diagnoses and diagnosis-related groups different comorbidities were identified. RESULTS: We studied a total of 45 365 admissions among patients with AC. The absolute number of admissions decreased from 2002 to 2014 (3866-2834 admissions). In-hospital mortality was variable throughout study duration without a clinically relevant trend (Mean 4.5%, range 3.6%-5.6%). The patients were mostly male (87%) and Caucasian (50.5%). Commonest age groups involved were 45-59 years (46.7%) followed by 60-74 years (29.2%). Trends in associated comorbidities such as smoking, drug abuse, depression, and hypertension increased over the same time period. Among all admissions, almost half were for cardiovascular etiologies (48.9%) and heart failure (≈24%) was the commonest reason for hospital admission. CONCLUSION: While the overall admissions among patients with AC decreased over time, the proportion of patients with high-risk characteristics such as smoking, depression, and drug abuse increased. Patients aged 45 and older were largely affected and cardiovascular etiologies predominated among causes for admission.

Acute reversible left ventricular dysfunction secondary to alcohol.

Chronic excess alcohol use is a well-established cause of dilated cardiomyopathy. The clinical features are variable because patients may be asymptomatic despite there being evidence of severe left ventricular dysfunction. Although the mechanism of alcohol-induced cardiomyopathy is not clearly understood, abstinence from alcohol has been associated with improvement in left ventricular function. Conversely, patients with ongoing alcohol abuse and dilated cardiomyopathy have a poor prognosis, with progressive biventricular failure and, ultimately, death. A case of rapid reversal of alcohol-induced cardiomyopathy with abstinence is reviewed. The present case highlights the acute toxic nature of alcohol and the potential for rapid functional recovery.

Alcoholic cardiomyopathy: What is known and what is not known.

Excessive alcohol consumption represents one of the main causes of non-ischemic dilated cardiomyopathy. Alcoholic cardiomyopathy is characterized by dilation and impaired contraction of one or both myocardial ventricles. It represents the final effect of alcohol-induced toxicity to the heart. Several pathophysiological mechanisms have been proposed at the basis of alcohol-induced damage, most of which are still object of research. Unfortunately, symptoms of alcoholic cardiomyopathy are not specific and common to other forms of heart failure and appear when dilatation and systolic dysfunction are consolidated. Thus, early diagnosis is mandatory to prevent the development and progression to heart failure. Although physicians are aware of this disease, several pitfalls in the diagnosis, natural history, prognosis and treatment are still present. The aim of this narrative review is to describe clinical characteristics of alcoholic cardiomyopathy, highlighting the areas of uncertainty.

The Wearable Cardioverter Defibrillator in Nonischemic Cardiomyopathy: A US National Database Analysis.

BACKGROUND: The wearable cardioverter defibrillator (WCD) is often used in patients at risk of sudden cardiac death (SCD) who are not yet candidates for an implantable cardioverter defibrillator (ICD). Newly diagnosed cardiomyopathy may be reversible, and a WCD may protect patients during the initial period of risk. We evaluate the benefit and compliance of the WCD in patients with nonischemic cardiomyopathy (NICM). METHODS: We reviewed a national database of patients with NICM who used WCDs and who self-reported a history of excess alcohol use, although other causes of cardiomyopathy could not be excluded. The database contained demographic data, initial ejection fraction (EF), reason for WCD prescription, compliance and use data, any detected arrhythmias, therapies, and reason for discontinuing WCD. Statistical analyses were performed using SAS, version 9.3 (SAS Institute, Cary, NC). RESULTS: Of the 127 patients, 88% were men with a mean age of 52.6 ± 11.0 years. The mean initial EF was 19.9% ± 7.4%. Patients wore the WCD for a median of 51 days and a median daily use of 18.0 hours per day. The most common reasons for discontinuing the WCD were improvement in EF (33%) or ICD implantation (23.6%). Seven patients (5.5%) had 9 sustained ventricular arrhythmia events, which were successfully treated with 100% conversion. There were 11 deaths (8.6%) during 100 days of follow-up. No deaths resulted from WCD shock failure or undersensing. CONCLUSIONS: NICM may have a significant risk of ventricular arrhythmias and death in the first few months. The WCD delivered appropriate therapy in 5.5% of patients. This study suggests that a WCD may be effective temporary prophylaxis for prevention of SCD in patients with newly diagnosed NICM.

Gated radionuclide angiocardiography in the noninvasive evaluation of a partially reversible alcoholic cardiomyopathy.

Serial gated radionuclide angiocardiography was used to demonstrate partial reversal of alcoholic cardiomyopathy, following abstention from alcohol. Six months subsequent to total abstention, the resting ejection fraction, which is a sensitive index of left ventricular function, increased from 19 percent to 42 percent. Thirteen months following total abstention, the resting ejection fraction was preserved at 40 percent. During stress, the ejection fraction increased to 53 percent. The clinical implication of this case report is that gated radionuclide angiocardiography may be used to noninvasively evaluate accurately the subsequent course of reversible alcoholic cardiomyopathy.

Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology.

In the United States, in both sexes and all races, long-term heavy alcohol consumption (of any beverage type) is the leading cause of a nonischemic, dilated cardiomyopathy, herein referred to as alcoholic cardiomyopathy (ACM). ACM is a specific heart muscle disease of a known cause that occurs in two stages: an asymptomatic stage and a symptomatic stage. In general, alcoholic patients consuming > 90 g of alcohol a day (approximately seven to eight standard drinks per day) for > 5 years are at risk for the development of asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. ACM is characterized by an increase in myocardial mass, dilation of the ventricles, and wall thinning. Changes in ventricular function may depend on the stage, in that asymptomatic ACM is associated with diastolic dysfunction, whereas systolic dysfunction is a common finding in symptomatic ACM patients. The pathophysiology of ACM is complex and may involve cell death (possibly due to apoptosis) and changes in many aspects of myocyte function. ACM remains an important cause of a dilated cardiomyopathy, and in latter stages can lead to heart failure. Alcohol abstinence, as well as the use of specific heart failure pharmacotherapies, is critical in improving ventricular function and outcomes in these patients.

Reversal of alcoholic cardiomyopathy in a patient with severe coronary artery disease.

Alcohol is a known cause of cardiomyopathy. Although the mechanism is not clearly understood, abstinence prior to the onset of fibrosis has been associated with improvement in left ventricular function. As shown in this report, the presence of severe coronary artery disease should not exclude other causes of left ventricular dysfunction, especially alcoholic cardiomyopathy.

Alcoholic heart disease: a review.

The association between chronic alcohol consumption and alcoholic heart disease in human beings is well recognized. Chronic alcohol consumption is the leading cause of secondary cardiomyopathy, a heart muscle disease associated with long-term alcohol consumption. Both acute and chronic alcohol consumption have a negative inotropic effect on the myocardium, precipitate arrhythmias, and may provoke angina pectoris. There are numerous reports that alcohol changes many subcellular processes that are involved in excitation-contraction coupling. However, the exact mechanism(s) underlying these changes in the heart are still poorly understood. Despite the recent presumptive protective reports that moderate alcohol consumption protects against the risk of coronary artery disease, nurses and physicians must educate all patients about the many other adverse effects of alcohol on the cardiovascular system. The purpose of this article is to review and discuss the mechanism(s) that may underlie changes in contractile function after long-term alcohol consumption and identify current trends in identification and treatment of alcoholic heart disease.

[Reversibility of alcoholic myocardiopathy with abstinence: presentation of 2 cases]. / Reversibilidad de la miocardiopatía alcohólica con la abstinencia: presentación de dos casos.

The sustained alcohol intake results in the development of a dilated cardiomyopathy; its pathogenesis and prognostic and evolutive factors have not yet been completely defined. It is classically considered that alcoholic cardiomyopathy has a poor prognosis, as two thirds of patients die within three years. However, in recent years some isolated cases of clinical reversibility after short abstinence periods have been reported without identification of the involved factors. Two chronic alcoholic patients are reported with congestive heart failure at admission; a diagnosis of alcoholic cardiomyopathy was made after cardiac catheterization and endomyocardial biopsy. The morphometric study of endomyocardial biopsy showed a preservation of the myofibrillary fraction with mild fibrosis. The clinical outcome was favorable: after three months of alcoholic abstinence, a complete clinical recovery with definite improvement of echocardiographic parameters and left ventricular ejection fraction in the radionuclide ventriculography were observed. Finally, the factors that appear to be involved in the presence or absence of reversibility of this type of cardiomyopathy are discussed.

Ethanol and heart disease. An underestimated contributing factor.

With the number of chronic heavy users of ethanol in the United States estimated to be 15 to 20 million and the evidence increasing that ethanol causes serious cardiac metabolic disturbances, ethanol abuse is obviously a serious problem and most likely is an important contributing factor to cardiac morbidity and mortality. However, a direct cause-and-effect relationship between the biochemical dysfunctions produced by ethanol and the clinical entity of alcoholic cardiomyopathy has not been clearly established. What is lacking is a method to differentiate the damage secondary to ethanol abuse from that secondary to other causes. Sorely needed is a biochemical or anatomic marker (perhaps evaluated by serial myocardial biopsy) for alcoholic cardiomyopathy and a study to detect which cases of dilated cardiomyopathy indeed are due to ethanol-induced damage. Further longterm studies are also needed to demonstrate the benefits of abstinence upon large groups of patients, the effects of abstinence upon sudden death, and the effects of discontinuance of ethanol use for patients in the early stages of alcoholic cardiomyopathy. Ethanol is probably an underestimated contributing factor to cardiac disease. The importance of determining ethanol's impact on cardiovascular morbidity and mortality is underscored by the facts that alcoholic heart disease is completely avoidable and is largely reversible by abstinence.

[Significance of alcohol abstinence in alcoholic cardiomyopathy with moderate left ventricular dysfunction]. / O significado da abstinência do alcool na cardiomiopatia alcoólica com disfunção ventricular moderada.

PURPOSE: To evaluate the role of a 12 month alcohol abstinence period in patients with moderate left ventricular dysfunction treated with anticongestive therapy. METHODS: Prospective observational study with 20 patients with alcoholic cardiomyopathy (ACM), 9 (45%) in functional class (FC) II and 11 (55%) in FC III, 16 (80%) men, mostly black (55%), from 35 to 56 (x = 45) years old, heavy alcohol users (> 80 g ethanol for 51 to 112 (x = 88) months. At the beginning, all agreed to participate with psychotherapy and clinical evaluation. After 12 months, they were divided in G-I, formed by those who remained abstemious and G-II of non-abstemious. RESULTS: After 12 months, among the 11 (55%) who remained in psychotherapy, 8 were in G-I, among those who did not 9 (45%), only 2 (22.22%) remained abstemious (G-I). At the end of the evaluation period, both groups had the same number of patients. Comparing them, we observed: a) lower mean systolic and diastolic left ventricular diameters in G-I; b) more hospitalizations in G-II (3); c) more patients with stable or better clinical evaluation in G-I. CONCLUSION: Despite the initial will, only 50% reached abstinence. When it was reached, patients had a better evolution in left ventricular systolic diameter and abstinence should always be tried even in the presence of moderate left ventricular dysfunction.

Alcoholic cardiomyopathy: pathophysiologic insights.

Alcoholic cardiomyopathy (ACM) is a specific heart muscle disease found in individuals with a history of long-term heavy alcohol consumption. ACM is associated with a number of adverse histological, cellular, and structural changes within the myocardium. Several mechanisms are implicated in mediating the adverse effects of ethanol, including the generation of oxidative stress, apoptotic cell death, impaired mitochondrial bioenergetics/stress, derangements in fatty acid metabolism and transport, and accelerated protein catabolism. In this review, we discuss the evidence for such mechanisms and present the potential importance of drinking patterns, genetic susceptibility, nutritional factors, race, and sex. The purpose of this review is to provide a mechanistic paradigm for future research in the area of ACM.

Alcoholic cardiomyopathy.

The myocardial depressant effects of excessive ethanol consumption have long been known. Excessive alcohol intake is reported in a wide range (3-40%) of patients with idiopathic dilated cardiomyopathy; furthermore, chronic excessive alcohol consumption may lead to progressive and chronic cardiac dysfunction and can be a possible cause of dilated cardiomyopathy, referred to as alcoholic cardiomyopathy (ACM). The pathophysiological mechanisms underlying ACM are poorly understood. Excessive alcohol consumption has been associated with left-ventricular myocyte loss in some animal models but not in all studies. In addition, heavy drinking may cause myocyte dysfunction, due to abnormalities in calcium homeostasis, and cause elevated levels of norepinephrine. Increasing doses of ethanol have been associated with a negative inotropic effect on myocytes in animal experiments. In this review, we evaluate the epidemiology, current pathophysiological mechanisms and possible role of factors that influence ACM and discuss its clinical presentation, prognosis and treatment.