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 association between alcohol-induced cardiomyopathy and myocarditis is controversial. In one six-patient study (12) focusing on alcoholic cardiomyopathy, the surprising histological findings on endomyocardial biopsy of two patients was found to be myocarditis with lymphocytic infiltration in association with myocyte degeneration or focal necrosis. However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this.

LIMITATIONS OF ACM STUDIES

• For a comprehensive overview see Table 2 with combined data from 6, 8, 24, 28.
• Basic research studies have described an abundance of mechanisms that could underscore the functional and structural alterations found in ACM.
• They found that 2 of the 6 individuals (33%) whose alcohol consumption exceeded 125 mL/d had cardiomegaly.
• Once the damage is considered irreversible, it’s difficult for the heart and rest of the body to recover.

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. Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction. 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. Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation. Most common age population for ACM is males from age with significant history of alcohol use for more than 10 years.

National trends in hospitalizations and outcomes in patients with alcoholic cardiomyopathy

During the first half of the 20th century, the concept of beriberi heart disease (ie, thiamine deficiency) was present throughout the medical literature, and the idea that alcohol had any direct effect on the myocardium was doubted. Epidemics of heart failure in persons who had consumed beer contaminated with arsenic in the 1900s and cobalt in the 1960s also obscured the observation that alcohol could exhibit a direct toxic effect. In the 1950s, evidence began to emerge that supported the idea of a direct toxic myocardial effect of alcohol, and research during the last 35 years has been particularly alcoholic cardiomyopathy symptoms productive in characterizing the disease entity of alcoholic cardiomyopathy (AC). Based on epidemiological evidence, ACM is recognized as a significant contributor to non-ischemic DCM in Western countries. 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.

Basic studies on molecular mechanisms of myocardial damage

Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption. Individuals with certain mitochondrial deoxyribonucleic acid (DNA) mutations and angiotensin-converting enzyme (ACE) genotypes (DD genotype) may be particularly susceptible to the damaging effects of alcohol. The effect measure for each outcome was conducted using the mean differences effect measure, where the outcomes were assessed in identical units across the various literature reviews used in the study.

Histologic Findings

In conditions of acute alcohol toxicity, ethanol has been shown to increase circulating catecholamine, which may play a role in myocardial damage. 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. Excessive intake of alcohol may result in increased systemic blood pressure in a dose-response relationship, and this may contribute to chronic myocardial dysfunction. Patients who consume more than two drinks per day have a 1.5- to 2-fold increase in hypertension compared with persons who do not drink alcohol, and this effect is most prominent when the daily intake of alcohol exceeds five drinks. Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy. Counseling and resource provision for patients should be part of management.