However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this. It is likely that those two patients were incorrectly labelled with alcohol-induced cardiomyopathy. Most common age population for ACM is males from age with significant history of alcohol use for more than 10 years. Females constitute roughly 14 % of cases of alcohol induced cardiomyopathy however lifetime exposure required for women to develop alcohol induced cardiomyopathy is less compared to men.

Cardiovascular risks and benefits of moderate and heavy alcohol consumption

The end-systolic dimension was 4.1 cm and the end-diastolic dimension was 5.0 cm (Figure 1). Diastolic dysfunction is the earliest sign of ACM and is usually seen in approximately 30% of patients with a history of chronic alcohol abuse with no evidence of systolic dysfunction nor left ventricle hypertrophy. Cardiomyopathy (CM) is a disease of the heart muscle, which can progressively worsen and ultimately lead to chronic congestive heart failure (CHF). As such, CMs are typically treated with a standard CHF pharmacological regimen in addition to mechanical circulatory support devices or orthotopic heart transplantation in severe refractory cases.

• It is important to note that these guidelines apply to healthy adults and should be adjusted for individuals with certain health conditions or those taking specific medications.
• If the left ventricular ejection fraction (LVEF) is less than or equal to 40%, this may also comprise a combination of angiotensin blocker-neprilysin inhibitor, diuretics, beta-blockers, diuretics, aldosterone receptor antagonists, and an angiotensin-converting enzyme inhibitor.
• Diagnosing ACM still relies on exclusion criteria, similar to alcoholic liver disease, as excessive alcohol consumption is observed in up to 40% of DCM patients.
• Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time13.
• As the pathogenesis of AC is complex, specific treatments focus on different targets.
• Alcoholic cardiomyopathy is a leading cause of non-ischemic dilated cardiomyopathy in United States.

Role of autophagy and regulatory mechanisms in alcoholic cardiomyopathy

• The prognosis of ACM can also depend on the presence of other comorbidities such as diabetes, hypertension, and obesity.10 These conditions can exacerbate the effects of ACM on the heart and increase the risk of complications.10 Therefore, it is important to manage these comorbidities to improve the overall prognosis of ACM.
• Also, current common cardiac therapies such as ICD and CRT devices were not used because of the period when the study was conducted.
• Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported.
• Another nutritional factor classically involved in the pathophysiology of AC was cobalt excess.

It is also likely that the actual rate of AC may be underestimated because of undercoding given that a number of patients would present as heart failure exacerbations, thereby altering code used. In addition to this, there is difficulty in actually making the diagnosis of AC itself clinically due to absence of specific diagnostic criteria and the need to rule out other causes of cardiomyopathy as well. However, looking into a big population database might be a good way to study such a difficult to diagnose disease process. We were unable to do any subgroup analysis especially to look into whether there is increased mortality among certain population subsets such as those with hypertension and coronary artery disease.

Pathogenesis of alcohol-induced cardiomyopathy

Metabolic CM is a secondary CM that results from disturbed energy production leading to impaired cardiac function. It may be caused by a myriad of endocrine disorders, familial storage diseases, and/or nutritional deficiencies. We have chosen to specifically focus on how the imbalance in thyroid hormones might lead to reversible cardiac dysfunction. Fauchier et al11 found that after 47 mo of follow-up, the transplant-free survival of DCM patients was better than that of patients with ACM, but these differences were no longer significant when comparing the DCM group with the alcoholics who refrained from drinking or significantly reduced their alcohol consumption11. The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al69 in 1971.

Treatment of alcohol-induced cardiomyopathy

There is evidence of premature ventricular contractions (PVCs) leading to CM, in which a patient with a reduced LVEF with over 56,000 PVCs per day was successfully ablated and had normalization of LV systolic function.17 Though ablation offers effective results, there is concern that it may not offer a permanent solution. In a study by Ling et al, 18 subjects with tachycardia-induced CM underwent successful radiofrequency ablation and subsequently had an increase in LVEF within 3 months. 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. The achievement of total alcohol abstinence represents the most effective strategy for the treatment of alcohol-induced ogan damage, including 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. A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24.

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. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding65.

There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction. Previous studies were conducted on rats that are fed alcohol for about eight months. They found alcoholic cardiomyopathy symptoms that there is about 14% loss of myocardial cells in the left ventricle of those rats. It showed a significant increase in both acute and chronic alcohol intoxication. All previous mechanisms can induce myocyte apoptosis through the induction of mitochondrial damage and oxidative stress 12.

According to several articles, even moderate alcohol use has comparable effects to abstinence. Goal-directed heart failure therapy, as utilized in idiopathic DCM with low ejection fraction, should be a part of pharmaceutical therapy. If the left ventricular ejection fraction (LVEF) is less than or equal to 40%, this may also comprise a combination of angiotensin blocker-neprilysin inhibitor, diuretics, beta-blockers, diuretics, aldosterone receptor antagonists, and an angiotensin-converting enzyme inhibitor. Some studies have shown that the combination of carvedilol and trimetazidine with other traditional heart failure medications is effective 1-3,7-11,16-20. Evidence of altered bioenergetics or mitochondrial dysfunction has been observed in various investigations of ethanol effect on the heart. Disrupted bioenergetics and oxidative phosphorylation indices and a change in the ultrastructure of the mitochondria may be the cause of such dysfunctions.

Through a thematic synthesis, we identified common trends, knowledge gaps, and emerging research areas related to ACM. To assess the quality and validity of the included studies, we performed a critical appraisal using appropriate tools such as the Newcastle-Ottawa Scale for observational studies or the Cochrane Risk of Bias tool for clinical trials. This assessment allowed us to evaluate the methodological rigor of each study and determine its overall quality and potential impact on the literature review. Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM. By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies.

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Alcohol results in acute as well as chronic depression of myocardial contractility, even when ingested by normal individuals in quantities consumed during social drinking.23 Compensatory mechanisms such as vasodilation or sympathetic stimulation may mask the direct acute myocardial depressant effects of alcohol. Alcohol (ethanol) is contained in a number of beverages consumed all over the world since ancient times. The acute ingestion of large amount of alcohol as well as chronic alcohol abuse induce toxic effects to all organs and tissues 7, particularly to central nervous system, liver and heart 8,9.