Alcoholic Cardiomyopathy (ACM) 

Alcoholic cardiomyopathy (ACM) is a non-ischemic dilated cardiomyopathy caused by chronic heavy alcohol consumption. It is a potentially reversible cause of heart failure if detected early and alcohol abstinence is achieved.


1️⃣ What is Alcoholic Cardiomyopathy?

Alcoholic cardiomyopathy is a form of toxic dilated cardiomyopathy characterized by:

  • LV dilation
  • Reduced systolic function ( EF)
  • Global hypokinesia
  • Progressive heart failure
  • Arrhythmias

It falls under non-ischemic cardiomyopathy in major heart failure classifications including those of the American Heart Association (AHA) and European Society of Cardiology (ESC).


2️⃣ Epidemiology

  • 20–40% of non-ischemic dilated cardiomyopathy in Western populations
  • More common in men
  • Typically after:
    • 80–100 g ethanol/day
    • Duration ≥5–10 years


3️⃣ Pathophysiology – Mechanisms of Alcohol-Induced Myocardial Injury

Alcohol causes direct myocardial toxicity via multiple mechanisms:

1️⃣ Direct Myocyte Toxicity

  • Ethanol acetaldehyde accumulation
  • Oxidative stress ( ROS)
  • Lipid peroxidation
  • Myofibrillar degeneration

2️⃣ Mitochondrial Dysfunction

3️⃣ Impaired Calcium Handling

4️⃣ Neurohormonal Activation

  • RAAS activation
  • SNS overactivity
  • Progressive remodeling

5️⃣ Nutritional Deficiency

  • Thiamine deficiency (wet beriberi overlap)
  • Magnesium deficiency
  • Protein malnutrition

6️⃣ Myocardial Fibrosis

4️⃣ Structural & Hemodynamic Changes

Morphology

  • Dilated LV
  • Thin ventricular walls
  • Biatrial enlargement
  • Secondary MR/TR

Hemodynamics

  • EF (<40%)
  • LVEDP
  • Pulmonary capillary wedge pressure
  • Low cardiac output state

Advanced stages resemble end-stage dilated cardiomyopathy.


5️⃣ Clinical Presentation

A. Chronic Presentation (Most Common)

  • Progressive dyspnea
  • Orthopnea
  • PND
  • Pedal edema
  • Fatigue
  • Ascites (late)

B. Arrhythmias

  • Atrial fibrillation
  • Ventricular tachycardia
  • Sudden cardiac death

C. Acute Decompensated HF

Often triggered by:

  • Alcohol binge
  • Infection
  • Withdrawal
  • Tachyarrhythmia


6️⃣ Examination Findings

  • S3 gallop
  • Displaced apex beat
  • Holosystolic murmur (functional MR)
  • Elevated JVP
  • Hepatomegaly
  • Pulmonary crackles


7️⃣ Investigations

1️⃣ ECG

  • Sinus tachycardia
  • AF
  • Non-specific ST-T changes
  • QRS prolongation

2️⃣ Echocardiography (Diagnostic Cornerstone)

  • Dilated LV
  • Global hypokinesia
  • Reduced EF
  • Functional MR
  • RV dysfunction (advanced)


3️⃣ Cardiac MRI

  • LV dilation
  • Diffuse fibrosis
  • Late gadolinium enhancement (non-ischemic pattern)


4️⃣ Biomarkers

  • BNP / NT-proBNP
  • Mild troponin elevation
  • LFT abnormalities
  • Macrocytosis (MCV )


5️⃣ Coronary Angiography

Must exclude:

  • Ischemic cardiomyopathy

Exam tip:

Alcoholic cardiomyopathy is a diagnosis of exclusion.


8️⃣ Diagnostic Criteria 

  1. Dilated cardiomyopathy phenotype
  2. History of chronic heavy alcohol intake
  3. Exclusion of ischemic heart disease
  4. Improvement after abstinence supports diagnosis


9️⃣ Differential Diagnosis

  • Idiopathic dilated cardiomyopathy
  • Viral myocarditis
  • Tachycardia-induced cardiomyopathy
  • Thiamine deficiency cardiomyopathy
  • Peripartum cardiomyopathy
  • Genetic cardiomyopathy


🔟 Management – Guideline Directed

Management follows HFrEF protocol (AHA/ESC guidelines).


A. ABSOLUTE ALCOHOL ABSTINENCE (Most Important)

  • EF can improve significantly
  • Reverse remodeling possible
  • Survival dramatically improves

🔴 Continued drinking progressive deterioration


B. Guideline Directed Medical Therapy (GDMT)

According to ESC/AHA HFrEF guidelines:

1️⃣ ARNI (preferred)

Sacubitril–valsartan

or

ACE inhibitor / ARB


2️⃣ Beta-blocker

  • Carvedilol
  • Metoprolol succinate
  • Bisoprolol


3️⃣ Mineralocorticoid receptor antagonist

  • Spironolactone
  • Eplerenone


4️⃣ SGLT2 inhibitors

  • Dapagliflozin
  • Empagliflozin


5️⃣ Diuretics

  • For congestion control


C. Arrhythmia Management

  • AF anticoagulation (CHA₂DS₂-VASc)
  • ICD if:
    • EF ≤35% after 3 months optimal therapy
  • CRT if:
    • LBBB + QRS ≥150 ms


D. Advanced Therapy

  • LVAD
  • Heart transplant (if abstinent and eligible)


1️⃣1️⃣ Reversibility 

Improvement depends on:

Factor

Outcome

Early diagnosis

Good recovery

Complete abstinence

Significant EF improvement

Advanced fibrosis

Irreversible damage

Continued drinking

Progressive HF

🔴 EF may improve within 6–12 months of abstinence.


1️⃣2️⃣ Prognosis

Without abstinence:

  • 4-year mortality up to 50%

With abstinence:

  • Significant survival improvement
  • Reverse remodeling possible


1️⃣3️⃣ ICU Considerations 

Acute Decompensated HF

  • IV diuretics
  • Vasodilators
  • Inotropes if low output
  • NIV / mechanical ventilation if needed

Alcohol Withdrawal

  • Benzodiazepines
  • Thiamine before glucose
  • Monitor for arrhythmias

Cardiogenic Shock

  • Dobutamine
  • Norepinephrine if hypotensive
  • Mechanical support if refractory


1️⃣4️⃣ Alcohol vs Thiamine Cardiomyopathy 

Feature

Alcoholic CM

Wet Beriberi

EF

Reduced

High output initially

SVR

Normal/

Markedly

Thiamine response

Partial

Dramatic

Mechanism

Direct toxicity

Metabolic failure