We also searched the Cochrane database which produced no results, a finding consistent with the fact that we excluded reviews and meta-analysis, as detailed below. Methods 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. Although several studies have tried to estimate the exact prevalence of AC, available data are not conclusive [4]. The reported prevalence of alcoholic cardiomyopathy among Alcohol Addiction Unit patients varies between 21% and 32%, although it could be higher [13], [14]. A literature review using the PubMed database with the search terms ‘alcoholic cardiomyopathy’, ‘alcoholic heart disease’, was conducted up to January 2017.
Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI). As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol. The evidence gleaned from this systematic review builds on basic research, expanding nursing science and applied research, facilitating future conceptual development and theory testing specific to understanding this phenomenon in addiction.
New Treatment Strategies for Alcohol-Induced Heart Damage
Demakis et al[70] 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. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven.
The QRS duration, LVESD (left ventricular end-systolic dimension) and LVEDD were higher in the death group but the LVEF was lower in the patients of death group than those patients in the in the survival group. The achievement of total alcohol abstinence represents the most effective strategy for the treatment of alcohol-induced ogan damage, including alcoholic cardiomyopathy, alcoholic cardiomyopathy in order to promote the recovery of left ventricular dysfunction [4], [11]. However, the limit between reversible and non-reversible damage, in other words the “point of no-return”, is currently not known [12]. At histological evaluation, dilatation, myofibrillar necrosis and fibrosis are typically present, with a reduction of myofibrils and giant mytochondria [3].
3. Statistical analysis
Screening, selection, data extraction, and narrative synthesis were performed independently by three reviewers (LAF, DP and BDB). Differences in article selection, quality, and relevance were resolved by a consensus with a fourth independent reviewer (LL) for final determination. 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.
Thus, Nicolás et al[73] studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal. The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%).
Sex Differences in the Clinical Presentation and Natural History of Dilated Cardiomyopathy.
Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea. Palpitations and syncopal episodes can occur due to tachyarrhythmias seen in alcoholic cardiomyopathy. 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. Alcoholic cardiomyopathy (ACM) is a leading cause of non-ischaemic dilated cardiomyopathy (DCM) in tribal and non-tribal population.
