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American Journal of Cardiovascular Drugs

, Volume 9, Issue 3, pp 177–196 | Cite as

Cocaine Cardiotoxicity

A Review of the Pathophysiology, Pathology, and Treatment Options
  • Katharine Phillips
  • Adriana Luk
  • Gursharan S. Soor
  • Jonathan R. Abraham
  • Shaun Leong
  • Jagdish Butany
Review Article

Abstract

Cocaine is a powerful stimulant that gives users a temporary sense of euphoria, mental alertness, talkativeness, and a decreased need for food and sleep. Cocaine intoxication is the most frequent cause of drug-related death reported by medical examiners in the US, and these events are most often related to the cardiovascular manifestations of the drug. Once playing a vital role in medicine as a local anesthetic, decades of research have established that cocaine has the ability to cause irreversible structural damage to the heart, greatly accelerate cardiovascular disease, and initiate sudden cardiac death. Although pathologic findings are often reported in the literature, few images are available to support these findings, and reviews of cocaine cardiopathology are rare. We describe the major pathologic findings linked to cocaine abuse in earlier research, their underlying mechanisms, and the treatment approaches currently being used in this patient population.

A MEDLINE search was conducted to identify all English language articles from January 2000 to June 2008 with the subject headings and key words ‘cocaine’, ‘heart’, ‘toxicity’, and ‘cardiotoxicity’. Epidemiologic, laboratory, and clinical studies on the pathology, pathophysiology, and pharmacology of the effects of cocaine on the heart were reviewed, along with relevant treatment options. Reference lists were used to identify earlier studies on these topics, and related articles from Google Scholar were also included.

There is an established connection between cocaine use and myocardial infarction (MI), arrhythmia, heart failure, and sudden cardiac death. Numerous mechanisms have been postulated to explain how cocaine contributes to these conditions. Among these, cocaine may lead to MI by causing coronary artery vasoconstriction and accelerated atherosclerosis, and by initiating thrombus formation. Cocaine has also been shown to block K+ channels, increase L-type Ca2+ channel current, and inhibit Na+ influx during depolarization, all possible causes for arrhythmia. Additionally, cocaine use has been associated with left ventricular hypertrophy, myocarditis, and dilated cardiomyopathy, which can lead to heart failure if drug use is continued.

Certain diagnostic tools, including ECG and serial cardiac markers, are not as accurate in identifying MI in cocaine users experiencing chest pain. As a result, clinicians should be suspicious of cocaine use in their differential diagnosis of chest pain, especially in the younger male population, and proceed more cautiously when use is suspected.

Treatment for cocaine-related cardiovascular disease is in many ways similar to treatment for traditional cardiovascular disease. However use of β-receptor antagonists and class Ia and III anti-arrhythmics is strongly discouraged if the patient is likely to continue cocaine use, because of documented adverse effects.

The medical community is in urgent need of a pharmacologic adjunct to cocaine-dependence treatment that can deter relapse and reduce the risks associated with cardiovascular disease in these patients.

Keywords

Cocaine Sudden Cardiac Death Carvedilol Aortic Dissection Therapeutic Hypothermia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Notes

Acknowledgments

No sources of funding were used to assist in the preparation of this review. The authors have no conflicts of interest that are directly relevant to the content of this review. The authors wish to acknowledge the assistance of the Forensic Pathology Service, Ministry of the Solicitor General, Government of Ontario, Toronto, for illustration materials, and the generous support of the Department of Pathology, University Health Network (Toronto General Hospital), Toronto. The authors also wish to acknowledge Melissa Skarban, Department of Pathology, University Health Network (Toronto General Hospital), Toronto, for her valuable assistance in preparing this manuscript.

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Copyright information

© Adis Data Information BV 2009

Authors and Affiliations

  • Katharine Phillips
    • 1
  • Adriana Luk
    • 2
  • Gursharan S. Soor
    • 1
  • Jonathan R. Abraham
    • 1
  • Shaun Leong
    • 1
  • Jagdish Butany
    • 1
    • 3
  1. 1.Department of Pathology 11E-420Toronto General Hospital/University Health NetworkTorontoCanada
  2. 2.Department of MedicineToronto General Hospital/University Health NetworkTorontoCanada
  3. 3.Departments of Laboratory Medicine and Pathobiology, Faculty of MedicineUniversity of TorontoTorontoCanada

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