Alcoholic cardiomyopathy: an update European Heart Journal

Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported. The natural history and long-term prognosis studies of Gavazzi et al10 and Fauchier et al11 compared the evolution of ACM patients according to their degree of withdrawal. These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival alcoholic cardiomyopathy symptoms rates without a heart transplant. The uptrend for admissions among Caucasian patients, increased from approximately 40% to near 60% between 2002 and 2014. Both African American and Hispanic patients also saw slight uptrend in the proportion of patients admitted, but the absolute percent increase by 2014 was much smaller in comparison. Another study indicated a decrease in the general hospitalization rates in heart failure across all races over the past couple of years.17 These differences could be attributed to racial disparities in access to healthcare leading to different rates of utilization of healthcare services.

Data Availability Statement

The frequencies of CTP (Grade B, C), NYHA (class III/IV) classification, AF and AVB were higher in the death group and sinus rhythm was observed to be more in the patients of survival group. The QRS duration, LVESD and LVEDD were higher in the death group and LVEF was observed to be lower in the patients of death group than those in the survival group. We studied 290 patients with ACM who were evaluated in our institute between January 2013 and December 2016. 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. Alcoholic cardiomyopathy (ACM) is a leading cause of non-ischaemic dilated cardiomyopathy (DCM) in tribal and non-tribal population.

• A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups.
• For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function21,33.
• According to most studies, the alcohol consumption required to establish a diagnosis of ACM is over 80 g per day during at least 5 years9-12.
• Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers.
• Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports.

Authors and Affiliations

It is unknown whether individual susceptibility would be related to increased vulnerability at the myocardial level and/or to impaired alcohol metabolism. Unfortunately Lazarević et al23, as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction. Any benefits of alcohol consumption are likely driven by cardiovascular disease, because alcohol is known to cause cancer 66,67, liver disease 68, injuries 69, mental health issues 70–72 and cognitive impairment 73. Cardiovascular benefits of alcohol have been attributed to alcohol raising HDL-cholesterol, reducing coronary artery plaque, reducing coagulation and anti-oxidant properties 74–76.

Alcohol and atrial fibrillation: a sobering review

The status of all patients was followed up by telephone interview, outpatient clinic attendance, or hospitalization during the follow-up period. Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM. Because of this, their origin could be multifactorial and linked both to the alcohol molecule and to its main metabolite, acetaldehyde. Furthermore, Fernández-Solá et al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.

In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM19. This research received no specific grant from any funding agency in the public, commercial, or not-for-profit sectors. Follow-up was done by outpatient department visit, telephonic conversation or hospital admission. We did not directly include patient and public involvement (PPI) in this study, but the database used in the study was developed with PPI and is updated by a committee that includes patient representatives. Normally distributed variables are expressed as the means and standard deviations or percentages, whereas non-normally distributed variables are presented as the medians and interquartile ranges (IQRs).

A receiver operating characteristic (ROC) curve analysis was performed to optimize the cutoff point for discriminating between the 2 risk groups. For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence. Considering all the works conducted to date, it is clear that new studies on the natural history of ACM are needed, including patients treated with contemporary heart failure therapies. In light of the available data, new studies will help to clarify the current prognosis of ACM compared to DCM and to determine prognostic factors in ACM that might differ from known prognostic factors in DCM.

In fact, Brandt et al.54 observed that in ALDH2-deficient mice, the most important increase in mitochondrial superoxide levels (which is the major species of ROS) is due to acetaldehyde, not ethanol. By inhibiting NOX2 (the most important superoxide-producing enzyme) with apocynin, they observed a decrease in ethanol- and acetaldehyde-induced superoxide levels. Demakis et al70 in 1974 divided a cohort of 57 ACM patients according to the evolution of their symptoms during follow-up. The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened. However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease.