Cardiology > Cocaine-Related Cardiomyopathy 

Background

Cocaine-related cardiomyopathy is a form of non-ischemic cardiomyopathy caused by chronic cocaine use, resulting in structural and functional abnormalities of the myocardium. It most often presents as dilated cardiomyopathy with impaired systolic function, but can also involve hypertrophy, arrhythmias, and heart failure. It may also lead to secondary (functional) mitral regurgitation due to ventricular dilation and papillary muscle displacement. 

II) Classification/Types

By Cardiac Involvement: 

• • Dilated Cardiomyopathy (most common) 

• • Hypertrophic Response (due to transient hypertension) 

• • Restrictive Physiology (rare, due to fibrosis) 

• • Arrhythmogenic Cardiomyopathy (due to conduction abnormalities) 

By Temporal Pattern: 

• • Acute Toxicity: Myocardial stunning, vasospasm, infarction 

• • Chronic Toxicity: Progressive myocyte damage, fibrosis, and remodeling 

III) Pathophysiology 

Cocaine increases catecholamines by inhibiting norepinephrine and dopamine reuptake, resulting in vasoconstriction, tachycardia, hypertension, and increased myocardial oxygen demand. These effects contribute to ischemia, direct myocardial toxicity, and progressive fibrosis, which leads to impaired contractility and left ventricular dilation. This dilation displaces the mitral valve apparatus, resulting in secondary (functional) mitral regurgitation. 

IV) Epidemiology

• • Sex: More common in males 

• • Age: Typically presents in young to middle-aged adults (30s–50s) 

• • Geography: Urban settings, particularly in areas with high prevalence of cocaine use 

• • Comorbidities: HIV, hepatitis C, tobacco use, alcohol abuse, and other substance use disorders 

Etiology

I) Causes

• • Chronic cocaine use (intranasal, smoked, intravenous) 

• • Binge use or repeated vasospastic episodes 

• • Polysubstance abuse (e.g., alcohol, methamphetamine) 

• • Underlying predisposition (e.g., genetic cardiomyopathy, hypertension) 

II) Risk Factors

• • Long-term, high-dose cocaine use 

• • Male gender 

• • African American ethnicity 

• • Poor social support 

• • Co-existing cardiovascular risk factors (HTN, smoking, hyperlipidemia) 

• • HIV infection 

Clinical Presentation

I) History (Symptoms)

• • Fatigue, exertional dyspnea 

• • Orthopnea, paroxysmal nocturnal dyspnea 

• • Lower extremity swelling 

• • Palpitations, syncope 

• • Chest pain (can mimic ACS) 

• • History of cocaine use (ask directly and non-judgmentally) 

II) Physical Exam (Signs)

Vital Signs: 

• • Tachycardia 

• • Hypertension (early) or hypotension (advanced) 

Cardiac: 

• • Displaced apical impulse 

• • S3 gallop 

• • Holosystolic murmur at apex (functional MR) 

Pulmonary: 

• • Rales, wheezes (pulmonary edema) 

Peripheral: 

• • Elevated JVP 

• • Peripheral edema 

• • Hepatomegaly, ascites (right heart failure) 

Differential Diagnosis (DDx)

• • Ischemic cardiomyopathy 

• • Viral myocarditis 

• • Alcoholic cardiomyopathy 

• • Takotsubo cardiomyopathy 

• • Hypertensive heart disease 

• • Valvular disease 

• • Sarcoidosis 

• • HIV-associated cardiomyopathy 

Diagnostic Tests

Initial Tests: 

Transthoracic Echocardiogram (TTE): 

• • LV dilation, reduced EF 

• • Functional MR due to papillary muscle displacement 

• • RV dysfunction may be present 

Electrocardiogram (ECG): 

• • Sinus tachycardia 

• • LVH or conduction delays 

• • Arrhythmias (atrial fibrillation, ventricular tachycardia) 

Chest X-ray: 

• • Cardiomegaly 

• • Pulmonary congestion or edema 

Cardiac Biomarkers: 

• • Troponin: may be mildly elevated 

• • BNP/NT-proBNP: elevated in heart failure 

Cardiac MRI: 

• • Assesses fibrosis (late gadolinium enhancement) 

• • Helps differentiate from ischemic cardiomyopathy 

Urine Drug Screen: 

• • Confirms recent cocaine use 

Cardiac Catheterization: 

• • Excludes obstructive CAD 

• • May show normal coronaries despite ischemic symptoms 

Treatment

I) Medical Management

Heart Failure Management (Guideline-Directed Medical Therapy): 

• • ACE inhibitors/ARBs or ARNIs 

• • Beta-blockers (e.g., carvedilol) 

• • Mineralocorticoid receptor antagonists 

• • SGLT2 inhibitors 

• • Diuretics for volume overload 

• • Hydralazine + nitrates (if African American or intolerant to ACEi) 

Cessation of Cocaine Use: 

• • Essential for stabilization and recovery 

• • Referral to addiction services 

Rate Control/Antiarrhythmics: 

• • Beta-blockers with caution (avoid in acute cocaine toxicity) 

• • Amiodarone for ventricular arrhythmias 

Anticoagulation: 

• • If atrial fibrillation or LV thrombus present 

II) Interventional/Surgical

ICD: 

• • For secondary prevention in patients with sustained VT or cardiac arrest 

• • For primary prevention if LVEF ≤35% despite optimized therapy 

LVAD or Heart Transplant: 

• • In refractory cases unresponsive to medical therapy 

• • Requires documented abstinence from cocaine and substance abuse treatment 

Patient Education, Screening, Vaccines

• • Importance of complete cocaine cessation 

• • Avoid alcohol and other cardiotoxins 

• • Daily weight monitoring 

• • Low-sodium diet 

• • Adherence to GDMT and follow-up 

• • Referral to cardiac rehab and substance abuse counseling 

Vaccinations: 

• • Influenza annually 

• • Pneumococcal vaccines 

• • Hepatitis A and B 

• • COVID-19 vaccination 

Consults

• • Cardiology: Diagnosis and GDMT initiation 

• • Addiction Medicine: Long-term recovery and relapse prevention 

• • Electrophysiology: If arrhythmias or ICD indication 

• • Cardiothoracic Surgery/Transplant Team: Advanced heart failure 

• • Social Work: Support for housing, counseling, rehabilitation 

Follow-Up

• TTE every 3–6 months to monitor EF and mitral regurgitation 

• Monitor for medication adherence and side effects 

• Regular drug screening if in recovery 

• Surveillance for arrhythmias or worsening heart failure 

• Reinforce lifestyle modifications and avoid triggers 

• Consider cardiac rehab for functional improvement