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
- Dilated cardiomyopathy phenotype
- History of chronic heavy alcohol intake
- Exclusion of ischemic heart disease
- 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 |

