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Dilated cardiomyopathy secondary to chronic cocaine abuse: a case report
Chad J Cooper, Sarmad Said, Haider Alkhateeb
1Department of Internal Medicine, Paul L, Foster School of Medicine, Texas Tech University Health Sciences Center at El Paso, El Paso, Texas, USA. german.hernandez@ttuhsc.edu.
Insights
Cocaine abuse can cause severe heart problems, including dilated cardiomyopathy. Stopping cocaine use can significantly improve heart function and ejection fraction, highlighting the reversibility of this condition.
Area of Science:
- Cardiology
- Toxicology
- Internal Medicine
Background:
- Cocaine is a sympathomimetic drug with known cardiovascular risks.
- Cocaine abuse is linked to various cardiac complications, including hypertension and myocardial infarction.
- Dilated cardiomyopathy is a potential consequence of chronic cocaine use.
Observation:
- A 38-year-old male with hypertension presented with shortness of breath after 18 years of weekly cocaine use.
- Physical examination revealed hypertension, tachycardia, and a systolic murmur.
- Elevated Brain natriuretic peptide and positive urine toxicology confirmed cocaine use; echocardiogram showed dilated cardiomyopathy.
Findings:
- Cardiac catheterization ruled out an ischemic cause for the cardiomyopathy.
- Medical management and drug rehabilitation were initiated.
- After 5 months of cocaine cessation, the patient's ejection function improved significantly.
Implications:
- Cocaine-induced cardiomyopathy, though underreported, is a serious condition.
- Management is similar to other cardiomyopathies, but beta-blockers should be avoided.
- Myocardial dysfunction is reversible upon cessation of cocaine use, with follow-up testing recommended.
Background:
Cocaine is a potent sympathomimetic agent associated with the development of possible fatal cardiovascular complications. Dysrhythmias, acute myocardial infarction, hypertension and dilated cardiomyopathy are just some of many cardiovascular effects related to the abuse of cocaine.
Case Presentation:
A 38-year-old Hispanic male with a past medical history of hypertension presented with a chief complaint of progressive shortness of breath. The patient confessed to the use of cocaine for almost 18 years once per week. On examination he was hypertensive and tachycardic with a systolic murmur over the 5th intercostal space at the level of the left mid-clavicular line. Laboratory workup revealed an elevated Brain natriuretic peptide; urine toxicology was positive for cocaine. 2D-echocardiogram showed dilated cardiomyopathy. Cardiac catheterization excluded angioischemic cause. He was managed medically and subsequently discharged with drug rehabilitation. On follow-up diagnostic evaluation after 5 months of cocaine cessation, his ejection function improved significantly.
Conclusion:
The exact incidence of cocaine related cardiomyopathy is unknown and likely underreported. The clinical course is abrupt and comparatively similar to other types of cardiomyopathy. The management is like other forms of cardiomyopathy; however β-blockers should be avoided. The myocardial dysfunction is reversible with abstaining from additional cocaine ingestion. Non-invasive testing should be performed after several months to re-evaluate the treatment response.
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