Cardiology > Alcoholic Cardiomyopathy

Background

Alcoholic cardiomyopathy (ACM) is a form of dilated cardiomyopathy caused by chronic, excessive alcohol intake, leading to direct myocardial toxicity. This condition results in left ventricular dilation and systolic dysfunction, ultimately progressing to heart failure if untreated. 

II) Classification/Types 

By Etiology: 

• • Primary (Idiopathic): Direct toxic effect of alcohol and its metabolites on cardiac myocytes. 

• • Secondary: ACM with co-existing nutritional deficiencies (e.g., thiamine), or concomitant conditions such as hemochromatosis or viral myocarditis. 

By Duration and Severity: 

• • Subclinical ACM: Asymptomatic systolic dysfunction in chronic alcohol users. 

• • Overt ACM: Symptomatic heart failure with reduced ejection fraction (HFrEF) due to long-standing alcohol abuse. 

By Alcohol Consumption Pattern: 

• • Chronic excessive use: Regular intake >80 g/day for >5 years. 

• • Binge drinking: Acute cardiac depression following massive single intake. 

III) Pathophysiology 

Ethanol and its metabolite acetaldehyde impair mitochondrial function, increase oxidative stress, and disrupt calcium homeostasis in cardiac myocytes. Chronic exposure leads to myocyte apoptosis, interstitial fibrosis, and impaired contractility. Neurohormonal activation (e.g., sympathetic nervous system, RAAS) further exacerbates remodeling and heart failure. 

IV) Epidemiology 

• • Sex: More common in men; however, women are more sensitive to alcohol toxicity. 

• • Age: Most commonly diagnosed in individuals aged 35–60. 

• • Geography: Higher prevalence in regions with high per capita alcohol consumption. 

• • Comorbidities: Often coexists with liver disease, hypertension, arrhythmias, or malnutrition. 

Etiology

I) Causes 

• • Chronic heavy alcohol consumption 

• • Binge drinking in genetically susceptible individuals 

• • Nutritional deficiencies (especially thiamine) 

• • Genetic predisposition to alcohol toxicity 

• • Concurrent liver cirrhosis or viral hepatitis 

II) Risk Factors 

• • Daily ethanol intake >80 g for ≥5 years 

• • Male gender 

• • Family history of cardiomyopathy 

• • Low socioeconomic status 

• • Poor nutritional status 

• • Smoking or other substance use 

• • Lack of access to preventive healthcare 

Clinical Presentation

I) History (Symptoms) 

• • Progressive dyspnea on exertion 

• • Orthopnea and paroxysmal nocturnal dyspnea 

• • Fatigue, weakness, reduced exercise capacity 

• • Palpitations (often due to atrial fibrillation) 

• • Peripheral edema, abdominal distension 

• • History of chronic alcohol use 

• • Rarely, chest pain or syncope 

II) Physical Exam (Signs) 

Vital Signs: 

• • Tachycardia 

• • Hypotension (advanced cases) 

• • Irregularly irregular rhythm (atrial fibrillation) 

Cardiac Exam: 

• • Displaced, diffuse apical impulse 

• • S3 gallop (volume overload) 

• • Holosystolic murmur (functional MR from dilation) 

Pulmonary: 

• • Bibasilar rales 

• • Possible pleural effusion 

Peripheral: 

• • Elevated jugular venous pressure 

• • Hepatojugular reflux 

• • Peripheral edema 

• • Ascites in coexisting cirrhosis 

Differential Diagnosis (DDx)

• • Dilated cardiomyopathy (non-alcoholic) 

• • Ischemic cardiomyopathy 

• • Viral myocarditis 

• • Hypertensive heart disease 

• • Restrictive cardiomyopathy 

• • Hemochromatosis 

• • Thyroid disease (hypo-/hyperthyroidism) 

• • Peripartum cardiomyopathy 

• • Beriberi heart disease (wet beriberi) 

Diagnostic Tests

Initial Tests: 

Transthoracic Echocardiogram (TTE): 

• • • Dilated LV with global hypokinesis 

• • • Reduced ejection fraction (usually <40%) 

• • • Functional mitral regurgitation 

• • • Rule out valvular pathology 

Electrocardiogram (ECG): 

• • • Sinus tachycardia or atrial fibrillation 

• • • Low voltage QRS (if pericardial effusion or coexisting liver disease) 

• • • Nonspecific ST-T changes 

Chest X-ray: 

• • • Cardiomegaly 

• • • Pulmonary congestion 

• • • Pleural effusions 

Cardiac MRI: 

• • • Confirms LV dilation, assesses fibrosis (late gadolinium enhancement) 

• • • Helps exclude infiltrative disease 

BNP/NT-proBNP: 

• • • Elevated in heart failure 

Liver Function Tests: 

• • • To assess coexisting liver damage 

Thiamine and nutritional panel: 

• • • Identify deficiencies (e.g., B1, folate) 

Alcohol biomarkers: 

• • • Carbohydrate-deficient transferrin (CDT), phosphatidylethanol (PEth) 

Treatment

I) Medical Management 

Alcohol Cessation: 

• • Cornerstone of treatment 

• • Can stabilize or improve cardiac function 

• • Referral to addiction counseling/rehab programs 

Heart Failure Management (HFrEF protocol): 

• • ACE inhibitors or ARBs 

• • Beta-blockers (e.g., carvedilol, metoprolol succinate) 

• • Mineralocorticoid receptor antagonists (e.g., spironolactone) 

• • SGLT2 inhibitors (e.g., dapagliflozin) 

• • Loop diuretics for volume overload 

• • Hydralazine + nitrates (in select patients) 

Arrhythmia Control: 

• • Rate control (beta-blockers, digoxin) 

• • Anticoagulation if atrial fibrillation and CHA₂DS₂-VASc ≥2 

• • ICD placement if EF <35% after 3 months of optimized therapy 

Nutritional Support: 

• • Thiamine supplementation 

• • Multivitamins and folate 

• • Dietary counseling 

II) Advanced/Interventional Options 

• • Cardiac resynchronization therapy (CRT) in LBBB with wide QRS 

• • ICD in patients with refractory ventricular arrhythmias or low EF 

• • Heart transplant in end-stage, non-recoverable cases (rare) 

Patient Education, Screening, Vaccines

• • Strong counseling on alcohol abstinence 

• • Explain link between alcohol and cardiac dysfunction 

• • Encourage fluid and sodium restriction in HF 

• • Daily weight monitoring to detect volume overload 

• • Educate on symptoms of decompensation (dyspnea, edema, fatigue) 

Vaccinations: 

• • Influenza annually 

• • Pneumococcal vaccine (PPSV23 and PCV15/20) 

• • Hepatitis A and B (if not immune) 

• • COVID-19 vaccination 

Consults

• • Cardiology: Diagnosis confirmation, EF monitoring, arrhythmia management 

• • Addiction Medicine: Alcohol cessation and relapse prevention 

• • Primary Care/Internal Medicine: Comorbidity optimization 

• • Nutritionist: Dietary and vitamin guidance 

• • Psychiatry: Dual-diagnosis management if depression/anxiety coexists 

• • Social Work: Support services and rehabilitation linkage 

Follow-Up

• • TTE every 3–6 months to monitor LV function post alcohol cessation 

• • Assess for improvement in EF and symptoms 

• • Monitor for arrhythmias, anticoagulation compliance 

• • Reinforce abstinence, screen for relapse 

• • Ongoing management of comorbidities (hypertension, liver disease)