ALCOHOL AND THE HEART: THE ROLE OF ETHANOL IN THE DEVELOPMENT OF CARDIOMYOPATHY AND HEART FAILURE
Abstract
Objective: Alcoholic cardiomyopathy (ACM) is a dilated cardiomyopathy resulting from chronic excessive alcohol consumption and is a preventable cause of heart failure. While moderate drinking was once thought to reduce cardiovascular risk, recent evidence suggests no safe threshold for ethanol intake. ACM typically develops after prolonged high-dose consumption, often >80 g/day for at least five years, though women may be affected at lower exposure. This review synthesizes epidemiological data, pathophysiology, clinical features, and therapeutic strategies related to ACM.
Methodology: This review synthesizes current evidence on ethanol’s cardiac effects and its role in ACM. A narrative synthesis of English-language studies from PubMed and Web of Science was performed, prioritizing systematic reviews, meta-analyses, randomized controlled trials, and large observational studies. Search terms included “alcoholic cardiomyopathy”, “cardiomyopathy”, “ethanol”, “alcohol”, and “heart failure”. Relevant studies were screened and qualitatively analyzed.
Key findings: Alcohol induces oxidative stress, mitochondrial dysfunction, impaired calcium handling, and disruption of sarcomeric proteins, culminating in progressive ventricular dilation, contractile dysfunction, fibrosis, and arrhythmias. Clinically, ACM progresses from asymptomatic ventricular dilation to overt systolic heart failure. Women are more susceptible, developing ACM at lower cumulative alcohol exposure than men.
Conclusion: ACM represents a preventable cause of heart failure, with early detection and alcohol cessation as critical components for improved outcomes. Public health efforts to reduce harmful drinking remain essential to decreasing ACM incidence and its cardiovascular burden.
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