Natural history and prognostic factors in alcoholic cardiomyopathy

Conversely, the 3 subjects recording a less satisfactory evolution had persisted Alcoholics Anonymous in their consumption of alcohol. It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition.

Natural History, Complications and Prognosis

In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility. More specifically, atrial fibrillation with rapid ventricular response is a cause of arrhythmia-induced cardiomyopathy,61 which can potentially worsen LVEF in AC patients, on top of the direct toxic effect of ethanol, acetaldehyde damage, or the aforementioned genetic factors. Among tribal population, no differences between the survival alcoholic cardiomyopathy is especially dangerous because and death groups were observed at the baseline in terms of age, sex, chest pain, basal crepts, orthopnoea, PND (paroxysmal nocturnal dyspnoea), JVP (jugular venous pressure), oedema and New York Heart Association (NYHA) classification. The frequencies of atrial fibrillation (AF), atrioventricular block (AVB) and CTP (Score B, C) were higher in the death group and sinus rhythm was observed to be more in the survival group.

Statistical analysis

The QRS duration, LVEDD and LVESD were higher but the LVEF was lower in the tribal population. The mainstay of management is providing support, resources including but not limited to alcoholic anonymous and encouragement for alcohol abstinence and address underlying stressors if any which requires assistance from nursing staff and pharmacy. Many changes can be observed including premature atrial or ventricular contractions, supraventricular tachycardias, atrioventricular blocks,  bundle branch blocks, QT prolongation, non-specific ST and T wave changes and abnormal Q waves.

Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy

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. Some studies have suggested that https://ecosoberhouse.com/ even moderation of alcohol consumption similar outcomes as compared to abstinence. Enzymatic activity changes which are seen in the idiopathic cardiomyopathy including decreased activity of oxygen reduction mitochondrial enzymes, increased fatty acid uptake and increased lysosomal/microsomal enzyme activity can be seen.

Study design and population

DCM, dilated cardiomyopathy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HTx, heart transplant; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; SD, standard deviation. Daily consumption of low to moderate amounts of alcohol has beneficial effects on cardiovascular health among both ischemic and non-ischemic patients1-3. In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF)3. Along with signs of heart failure such as increased N-terminal pro-B-type natriuretic peptide, blood tests can provide hints suggesting chronic alcohol abuse. Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease1,2. Ballester specifically analysed the effects of alcohol withdrawal on the myocardium using antimyosin antibodies labelled with Indium-11172.

• It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM44.
• Since those initial descriptions, reports on several isolated cases or in small series of patients with HF due to DCM and high alcohol intake have been published15-17.
• In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility.
• This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic).
• This section collects any data citations, data availability statements, or supplementary materials included in this article.

Correlation between independent predictors and all-cause mortality

Epidemiological studies analysing the relationship between excessive alcohol consumption and the development of DCM have found the existence of a reciprocal link between both disorders. Finally, it is worth stressing that a large majority of studies on the physiopathology and prognosis of ACM were conducted some years ago, prior to the development of our current understanding regarding the role of genetics in DCM67. According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases68.

This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%). The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies. Additionally, echocardiographic data suggest that subjects who do not fully withdraw from alcohol consumption, but who reduce it to moderate amounts recover LVEF in a similar manner to strict non-drinkers.

• Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM.
• Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction.
• Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century.

This study included not only DCM, but also all causes of left ventricular dysfunction, including hypertensive heart disease, ischemic cardiomyopathy and heart valve disease. Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). 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. However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years.

The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. In spite of the fact that alcohol plays a major role in the causation of DCM, very few studies have been published on the long-term outcome of patients with ACM in India and there is a major paucity of data comparing ACM in tribal and non-tribal population. This study was undertaken to find out the long-term outcome and prognostic markers of ACM and to compare the different characteristics of the patients between the death and survival groups in tribal and non-tribal population, simultaneously. In all ACM studies, inclusion of patients is based on patients’ self-reported alcohol drinking habits, which may lead to an underestimation of the prevalence of ACM together with problematic identification of patients who abstain and those who continue drinking. Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report.

Clinical profile

It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. Overall data with regards to alcohol induced cardiomyopathy is insuffienct and does not illustrate significant available data. Dilated cardiomyopathy secondary to alcohol use does not have a pre-defined exposure time. Daily alcohol consumption of 80 g per day or more for more than 5 years significantly increases the risk, however not all chronic alcohol users will develop Alcohol-induced cardiomyopathy. Future studies with a strict classification of non-drinkers and drinkers will help clarify whether complete abstinence is mandatory for ACM patients.