Alcoholic cardiomyopathy: an update.

Alcohol-induced cardiomyopathy (AC) is an acquired form of dilated cardiomyopathy (DCM) caused by prolonged and heavy alcohol intake in the absence of other causes. The amount of alcohol required to produce AC is generally considered as >80 g/day over 5 years, but there is still some controversy regarding this definition. This review on AC focuses on pathogenesis, which involves different mechanisms. Firstly, the direct toxic effect of ethanol promotes oxidative stress in the myocardium and activation of the renin-angiotensin system. Moreover, acetaldehyde, the best-studied metabolite of alcohol, can contribute to myocardial damage impairing actin-myosin interaction and producing mitochondrial dysfunction. Genetic factors are also involved in the pathogenesis of AC, with DCM-causing genetic variants in patients with AC, especially titin-truncating variants. These findings support a double-hit hypothesis in AC, combining genetics and environmental factors. The synergistic effect of alcohol with concomitant conditions such as hypertension or liver cirrhosis can be another contributing factor leading to AC. There are no specific cardiac signs and symptoms in AC as compared with other forms of DCM. However, natural history of AC differs from DCM and relies directly on alcohol withdrawal, as left ventricular ejection fraction recovery in abstainers is associated with an excellent prognosis. Thus, abstinence from alcohol is the most crucial step in treating AC, and specific therapies are available for this purpose. Otherwise, AC should be treated according to current guidelines of heart failure with reduced ejection fraction. Targeted therapies based on AC pathogenesis are currently being developed and could potentially improve AC treatment in the future.

A Pilot Metabolomic Study on Myocardial Injury Caused by Chronic Alcohol Consumption-Alcoholic Cardiomyopathy.

Chronic alcohol consumption leads to myocardial injury, ventricle dilation, and cardiac dysfunction, which is defined as alcoholic cardiomyopathy (ACM). To explore the induced myocardial injury and underlying mechanism of ACM, the Liber-DeCarli liquid diet was used to establish an animal model of ACM and histopathology, echocardiography, molecular biology, and metabolomics were employed. Hematoxylin-eosin and Masson's trichrome staining revealed disordered myocardial structure and local fibrosis in the ACM group. Echocardiography revealed thinning wall and dilation of the left ventricle and decreased cardiac function in the ACM group, with increased serum levels of brain natriuretic peptide (BNP) and expression of myocardial BNP mRNA measured through enzyme-linked immunosorbent assay and real-time quantitative polymerase chain reaction (PCR), respectively. Through metabolomic analysis of myocardium specimens, 297 differentially expressed metabolites were identified which were involved in KEGG pathways related to the biosynthesis of unsaturated fatty acids, vitamin digestion and absorption, oxidative phosphorylation, pentose phosphate, and purine and pyrimidine metabolism. The present study demonstrated chronic alcohol consumption caused disordered cardiomyocyte structure, thinning and dilation of the left ventricle, and decreased cardiac function. Metabolomic analysis of myocardium specimens and KEGG enrichment analysis further demonstrated that several differentially expressed metabolites and pathways were involved in the ACM group, which suggests potential causes of myocardial injury due to chronic alcohol exposure and provides insight for further research elucidating the underlying mechanisms of ACM.

Astaxanthin attenuates alcoholic cardiomyopathy via inhibition of endoplasmic reticulum stress-mediated cardiac apoptosis.

Chronic excessive ethanol consumption is associated with a high incidence of mortality due to ethanol-induced dilated cardiomyopathy, known as alcoholic cardiomyopathy (ACM). Mechanistic studies have demonstrated that apoptosis is key to the pathogenesis of ACM, and endoplasmic reticulum (ER) stress-associated apoptosis contributes to various ethanol-related diseases. Astaxanthin (AST) is a natural carotenoid that exerts an anti-ER stress effect. Importantly, strong evidence has shown that AST induces beneficial effects in various cardiovascular diseases. The present study aimed to investigate whether AST induces beneficial effects on ACM by suppressing cardiac apoptosis mediated by ER stress. We showed that after 2 months of chronic excessive ethanol consumption, mice displayed obvious cardiac dysfunction and morphological changes associated with increased fibrosis, oxidative stress, ER stress and apoptosis. However, cardiac damage above was attenuated in response to AST treatment. The cardioprotective effect of AST against ethanol toxicity was also confirmed in both H9c2 cells and primary cardiomyocytes, indicating that AST-induced protection directly targets cardiomyocytes. Both in vivo and in vitro studies showed that AST inhibited all three ER stress signaling pathways activated by ethanol. Furthermore, administration of the ER stress inhibitor sodium 4-phenylbutyrate (4-PBA) strongly suppressed ethanol-induced cardiomyocyte damage. Interestingly, AST induced further anti-apoptotic effects once co-treated with 4-PBA, indicating that AST protects the heart from ACM partially by attenuating ER stress, but other mechanisms still exist. This study highlights that administration of AST ablated chronic excessive ethanol consumption-induced cardiomyopathy by suppressing cardiac ER stress and subsequent apoptosis.

Clinical profile and prognostic factors of alcoholic cardiomyopathy in tribal and non-tribal population.

OBJECTIVE: Alcoholic cardiomyopathy (ACM) is a leading cause of non-ischaemic dilated cardiomyopathy (DCM) in tribal and non-tribal population. However, no study has been done depicting the correlation between clinical profile and prognosis of ACM in tribal and non-tribal population. This study also defines the long-term outcome and prognostic markers of ACM. METHODS: We studied 290 patients with ACM who were evaluated in our institute between January 2013 and December 2016. The primary endpoint of the study was all-cause mortality. Statistical analysis was done by using Kaplan-Meier survival curves for the assessment of all-cause mortality and Cox regression for the assessment of risk factors. RESULTS: After a median follow-up period of 3.75 years (IQR: 3-4 years), 50 patients with ACM (37.3%) died among tribal population while 14 patients (9%) died among non-tribal population. Independent predictors of all-cause mortality in ACM identified by Cox regression were left ventricular ejection fraction (LVEF) (HR: 0.883; 95% CI 0.783 to 0.996; p=0.043), QRS duration (HR: 1.010; 95% CI 1.007 to 1.017; p=0.005) and Child-Turcotte-Pugh (CTP) Scoring (HR: 12.332; 95% CI 6.999 to 21.728; p<0.001) at admission. The Kaplan-Meier survival probability estimate was 95.1% at 1 year and all-cause mortality was found to be higher in patients with QRS>120 ms, LVEF ≤35%, CTP Grade B/C than patients with QRS≤120 ms, LVEF >35% and CTP Score A, respectively (log-rank χ²=55.088, p<0.001; log-rank χ²=32.953, p<0.001; log-rank χ²=139.764, p<0.001, respectively). CONCLUSION: Our study indicated increased morbidity and mortality in tribal population. LVEF, QRS duration and CTP Scoring at the time of presentation were found to be the independent prognostic markers of patients with ACM.

The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy.

Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage. Ethanol induces ACM in a dose-dependent manner, independently of nutrition, vitamin, or electrolyte disturbances. It has synergistic effects with other heart risk factors. ACM produces a progressive reduction in myocardial contractility and heart chamber dilatation, leading to heart failure episodes and arrhythmias. Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis. Myocyte ethanol targets include changes in membrane composition, receptors, ion channels, intracellular [Ca2+] transients, and structural proteins, and disrupt sarcomere contractility. Cardiac remodeling tries to compensate for this damage, establishing a balance between aggression and defense mechanisms. The final process of ACM is the result of dosage and individual predisposition. The ACM prognosis depends on the degree of persistent ethanol intake. Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence.

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.

Specific Features of Depolarization of the Left and Right Atria in Rats with Alcoholic Cardiomyopathy.

Using a translation model of alcoholic cardiomyopathy in rats we showed the presence of an additional abnormal excitation focus in the area of the pulmonary vein lacunae in the left atrium and enhanced heterogeneity of the atrium depolarization pattern. These changes can determine electric instability of the myocardium and induce malignant heart rhythm disturbances including, sudden cardiac death.

Epac Proteins and Calmodulin as Possible Arrhythmogenesis Trigger in Alcoholic Cardiomyopathy.

The expression of Epac proteins (exchange protein directly activated by cAMP) and calmodulin (CaM) was assessed by the content of the corresponding mRNA in biopsy specimens of cardiac atrium, left ventricle, and thoracic aorta of rats with alcoholic cardiomyopathy. In the myocardium, overexpression of Еpac1, Ерас2, and СаМ mRNA was found. The content of Epac2 mRNA in the left ventricle was elevated by 2.9 times (p=0.000001), in the left atrium by 3.2 times (p=0.00001), in the right atrium by 3 times (p=0.00001). In contrast to the myocardial tissue, the content of CaM mRNA in the thoracic aorta was not increased, but showed a tendency to decrease, when compared to the control values, while the level of Epac1 and Epac2 mRNA was increased. The assumption is made that regulatory proteins Epac and CaM can play a key role in arrhythmogenesis development under conditions of alcoholic cardiomyopathy.

The Prognostic Factors of Alcoholic Cardiomyopathy: A single-center cohort study.

BACKGROUND: Alcoholic cardiomyopathy (ACM) is considered one of the main causes of left ventricular dysfunction and is the leading cause of nonischemic dilated cardiomyopathy (DCM) in developed countries. However, very few studies have investigated the relationship between clinical characteristics and prognosis in ACM. AIMS: This study aimed to identify risk factors related to a poor outcome in ACM patients. STUDY DESIGN: Retrospective cohort study. METHODS: This study included 321 patients with ACM admitted to our hospital between 2003 and 2013. This study aimed to investigate the clinical characteristics and outcomes of the patients with ACM, and the primary endpoint of the study was all-cause mortality, which was assessed through patient medical records (review of patient hospital records and periodic examination of patients in the outpatient clinic) and medical follow-up calls with trained personnel. All-cause mortality was assessed using Kaplan-Meier survival curves, and the risk factors were assessed using Cox regression. A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups. RESULTS: After a median follow-up period of 3.78 years (interquartile range: 2.08-6.52 years), 83 (27.7%) patients were dead. The independent predictors of all-cause mortality due to ACM were the QRS duration (HR: 1.014; 95% CI: 1.004-1.019; P = .003), systolic blood pressure (HR: 0.980; 95% CI: 0.963- 0.997; P = .020), and New York Heart Association classification (HR: 1.595; 95% CI: 1.110-2.290; P = .011) at admission. CONCLUSION: Our study indicated that the QRS duration, systolic blood pressure, and New York Heart Association classification at admission provided independent prognostic information in patients with ACM.

Reversibilidad de la miocardiopatía dilatada alcohólica / Reversibility of alcohol dilated cardiomyopathy

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Impacto pronóstico y factores predictores de la recuperación de la fracción de eyección en pacientes con miocardiopatía dilatada alcohólica / Prognostic impact and predictors of ejection fraction recovery in patients with alcoholic cardiomyopathy

Introducción y objetivos: La recuperación de la fracción de eyección del ventrículo izquierdo (FEVI) está descrita en la miocardiopatía alcohólica (MCA) tras la abstinencia alcohólica. Sin embargo, se desconoce el impacto pronóstico de esta recuperación y los factores con que se asocia. El objetivo es definir el papel pronóstico a largo plazo de la mejoría de la FEVI en la MCA e identificar sus predictores. Métodos: Se evaluó a 101 pacientes con MCA, con una mediana de seguimiento de 82 [intervalo intercuartílico, 36-134] meses. Resultados: Al final del seguimiento, 42 pacientes (42%) mostraron una recuperación significativa de la FEVI, definida como un incremento absoluto ≥ 10% y FEVI final ≥ 40%. Estos pacientes mostraron mejor pronóstico que aquellos sin recuperación de la FEVI (trasplante cardiaco o muerte cardiovascular, el 1 frente al 30%; p < 0,001). La duración del QRS < 120 ms (OR = 6,68; IC95%, 2,30-19,41), el tratamiento bloqueador beta (OR = 3,01; IC95%, 1,09-8,28) y no necesitar diuréticos (OR = 3,35; IC95%, 1,08-10,42) predijeron la recuperación de la FEVI en el análisis multivariable. Aunque el cese del consumo de alcohol no fue predictor, ninguno de los pacientes (n = 6) que mantuvieron un consumo excesivo recuperó la FEVI. Entre los abstemios y quienes mantuvieron un consumo moderado, hubo similar número de pacientes que recuperaron la FEVI (el 44 frente al 45%; p = 0,9). Conclusiones: La recuperación de la FEVI se asocia con un excelente pronóstico en la MCA. El tratamiento con bloqueadores beta, un QRS < 120 ms y no tomar diuréticos son predictores independientes de esta recuperación. La recuperación de la FEVI es similar entre bebedores moderados y abstemios

Introduction and objectives: Recovery of left ventricular ejection fraction (LVEF) has been described in alcoholic cardiomyopathy (ACM) after a period of alcohol withdrawal. Nevertheless, the prognostic impact of LVEF recovery in ACM and its determinants have not been studied. We sought to define the role of LVEF improvement in the long-term outcome of ACM and to identify predictors of LVEF recovery in these patients. Methods: We evaluated 101 ACM patients during a median follow-up period of 82 months [interquartile range 36-134]. Results: At latest follow-up, 42 patients (42%) showed substantial LVEF recovery defined as an absolute increase in LVEF ≥ 10% to a final value of ≥ 40%. Patients who recovered LVEF had better outcomes than patients who did not (heart transplant or cardiovascular death 1% vs 30%; P < .001). A QRS with < 120 ms (OR, 6.68; 95%CI, 2.30-19.41), beta-blocker therapy (OR, 3.01; 95%CI, 1.09-8.28), and the absence of diuretics (OR, 3.35; 95%CI, 1.08-10.42) predicted LVEF recovery in multivariate analysis. Although alcohol cessation did not predict LVEF recovery, none of the patients (n = 6) who persisted with heavy alcohol consumption recovered LVEF. The rate of patients who recovered LVEF did not differ between abstainers and moderate drinkers (44% vs 45%; P = .9). Conclusions: The LVEF recovery is associated with an excellent prognosis in ACM. Beta-blocker treatment, QRS < 120 ms and absence of diuretics are independent predictors of LVEF recovery. LVEF recovery is similar in moderate drinkers and abstainers

Atria Depolarization in Rats with Alcoholic Cardiomyopathy.

Chronotopography of atrial subepicardium depolarization has been studied in a rat model of alcoholic cardiomyopathy. Formation of independent sources of initial atrial activity has been detected in the right and left atria. These sources induced the formation of several depolarization fronts that propagated autonomously, and this can be regarded as the cause of atrial arrhythmia.

Prognostic Impact and Predictors of Ejection Fraction Recovery in Patients With Alcoholic Cardiomyopathy.

INTRODUCTION AND OBJECTIVES: Recovery of left ventricular ejection fraction (LVEF) has been described in alcoholic cardiomyopathy (ACM) after a period of alcohol withdrawal. Nevertheless, the prognostic impact of LVEF recovery in ACM and its determinants have not been studied. We sought to define the role of LVEF improvement in the long-term outcome of ACM and to identify predictors of LVEF recovery in these patients. METHODS: We evaluated 101 ACM patients during a median follow-up period of 82 months [interquartile range 36-134]. RESULTS: At latest follow-up, 42 patients (42%) showed substantial LVEF recovery defined as an absolute increase in LVEF ≥ 10% to a final value of ≥ 40%. Patients who recovered LVEF had better outcomes than patients who did not (heart transplant or cardiovascular death 1% vs 30%; P <.001). A QRS with <120ms (OR, 6.68; 95%CI, 2.30-19.41), beta-blocker therapy (OR, 3.01; 95%CI, 1.09-8.28), and the absence of diuretics (OR, 3.35; 95%CI, 1.08-10.42) predicted LVEF recovery in multivariate analysis. Although alcohol cessation did not predict LVEF recovery, none of the patients (n=6) who persisted with heavy alcohol consumption recovered LVEF. The rate of patients who recovered LVEF did not differ between abstainers and moderate drinkers (44% vs 45%; P=.9). CONCLUSIONS: The LVEF recovery is associated with an excellent prognosis in ACM. Beta-blocker treatment, QRS <120ms and absence of diuretics are independent predictors of LVEF recovery. LVEF recovery is similar in moderate drinkers and abstainers.

Inferolateral early repolarization among non-ischaemic sudden cardiac death victims.

Aim: Inferolateral early repolarization (ER) has been associated with an increased risk of sudden cardiac death (SCD). However, this association is thought to be mainly due to ischaemic SCD. The association of ER and non-ischaemic SCD has not been studied. The aim was to evaluate whether inferolateral ER is associated with non-ischaemic SCD. Methods and results: Study population consists of 275 consecutive victims of non-ischaemic SCD with 12-lead ECG and control group of general population cohort with 10 864 subjects. Sudden cardiac deaths were verified as non-ischaemic by medicolegal autopsy. Hypertensive cardiomyopathy (HTCMP) (25%), alcohol related dilated cardiomyopathy (ACMP) (24%), obesity associated cardiomyopathy (OCMP) (23%), and idiopathic myocardial fibrosis (IMF) (15%) were the most common causes of non-ischaemic SCD. A structurally normal heart was seen in only 1.5%. The prevalence of inferolateral ER was 20.7% among patients with non-ischaemic SCD compared to 5.3% in the general population (P < 0.001). The ECG pattern was accompanied with a horizontal/descending ST segment in 95% of the cases. The prevalence of inferolateral ER was slightly higher in the HTCMP group (26%) and the ACMP group (24%) than in the IMF group (20%) and the OCMP group (13%). The history of previously diagnosed cardiac diseases was not higher among subjects with ER (55%) than those without (59%, P = 0.59). Conclusion: The prevalence of inferolateral ER among non-ischaemic SCD victims is high. Almost all ER patterns are accompanied with the malignant horizontal/descending ST segment morphology suggesting that inferolateral ER is not only associated with an ischaemic SCD but also a non-ischaemic SCD.

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.

Alcoholic Cardiomyopathy: Disrupted Protein Balance and Impaired Cardiomyocyte Contractility.

Alcoholic cardiomyopathy (ACM) can develop after consumption of relatively large amounts of alcohol over time or from acute binge drinking. Of the many factors implicated in the etiology of ACM, chronic perturbation in protein balance has been strongly implicated. This review focused on recent contributions (since 2010) in the area of protein metabolism and cardiac function related to ACM. Data reviewed include that from in vitro and preclinical in vivo animal studies where alcohol or an oxidative metabolite was studied and outcome measures in either cardiomyocytes or whole heart pertaining to protein synthesis or degradation were reported. Additionally, studies on the contractile properties of cardiomyocytes were also included to link signal transduction with function. Methodological differences including the potential impact of sex, dosing, and duration/timing of alcohol administration are addressed. Acute and chronic alcohol consumption decreases cardiac protein synthesis and/or activation of proteins within the regulatory mammalian/mechanistic target of rapamycin complex pathway. Albeit limited, evidence suggests that myocardial protein degradation via the ubiquitin pathway is not altered, while autophagy may be enhanced in ACM. Alcohol impairs ex vivo cardiomyocyte contractility in relation to its metabolism and expression of proteins within the growth factor pathway. Dysregulation of protein metabolism, including the rate of protein synthesis and autophagy, may contribute to contractile deficits and is a hallmark feature of ACM meriting additional sex-inclusive, methodologically consistent studies.

Harm reduction-a systematic review on effects of alcohol reduction on physical and mental symptoms.

Based on the knowledge that alcohol misuse causes a multitude of diseases and increased mortality, this systematic review examines whether a reduction of the individual alcohol consumption can contribute to a minimization of health risks within a harm reduction approach. In fact, the reviewed 63 studies indicate that interventions aiming at alcohol reduction (including total abstinence as one possible therapeutic aim) indeed resulted in or were associated with positive effects in harmful, hazardous or alcohol-dependent drinkers. Major benefits were observed for reducing alcohol-associated injuries, recovery of ventricular heart function in alcoholic cardiomyopathy, blood pressure lowering, normalization of biochemical parameter, body weight reduction, histological improvement in pre-cirrhotic alcohol-related liver disease and slowed progression of an already existing alcohol-attributable liver fibrosis. Furthermore, reduced withdrawal symptoms, prevalence of psychiatric episodes and duration of in-patient hospital days, improvement of anxiety and depression symptoms, self-confidence, physical and mental quality of life, fewer alcohol-related adverse consequences as well as lower psychosocial stress levels and better social functioning can result from reduced alcohol intake. The reviewed literature demonstrated remarkable socioeconomic cost benefits in areas such as the medical health-care system or workforce productivity. Individuals with heightened vulnerability further benefit significantly from alcohol reduction (e.g. hypertension, hepatitis C, psychiatric co-morbidities, pregnancy, but also among adolescents and young adults). Concluding, the reviewed studies strongly support and emphasize the importance and benefits of early initial screening for problematic alcohol use followed by brief and other interventions in first contact medical health-care facilities to reduce alcohol intake.

[Cardiac damage in liver cirrhosis in alcohol abusers]. / Porazhenie serdtsa pri tsirroze pecheni u bol'nykh, zloupotreblyayushchikh alkogolem.

AIM: to estimate the contribution of liver cirrhosis (LC) to the development of heart diseases in alcohol abusers. SUBJECTS AND METHODS: The investigation included 80 patients with alcoholic LC without a history of cardiovascular and respiratory diseases and, as a control group, 32 alcohol abusers without a history of chronic diseases of the liver and cardiovascular and respiratory systems; 45 patients with alcoholic cardiomyopathy (ACM) and congestive heart failure without a history of coronary heart disease and valvular diseases, among whom 11 patients were found to have LC. In addition to standard clinical examination, all the patients underwent electrocardiography, by estimating the corrected QT interval (QTc), standard echocardiography; and those without ACM underwent estimation of left ventricular (LV) kinetics using speckle-tracking echocardiography. RESULTS: The patients with alcoholic LC were found to have a higher LV ejection fraction and a more obvious impairment of LV global longitudinal deformity, and more commonly LV diastolic dysfunction. 16 of the 80 patients with LC were observed to have moderate pulmonary hypertension while the mean pulmonary artery pressure (MPAP) was within the normal range in all the patients without LC. A prolonged QTc interval was revealed in the patients with LC. The duration of QTc was directly correlated with the MELD severity of LC. The patients with chronic heart failure in the presence of ACM and CL showed a more obvious LV diastolic dysfunction, as estimated by E/E', a greater LV mass index, and a higher MPAP than those with ACM without LC. CONCLUSION: The LC patients both with ACM and without a history of diseases of the heart were noted to have its more evident disorders as diastolic dysfunction and elevated MPAP. Those without ACM were observed to have impaired LV global deformity and a prolonged QTc interval.