Document Detail


Cocaine cardiotoxicity: a review of the pathophysiology, pathology, and treatment options.
MedLine Citation:
PMID:  19463023     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 beta-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.
Authors:
Katharine Phillips; Adriana Luk; Gursharan S Soor; Jonathan R Abraham; Shaun Leong; Jagdish Butany
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  American journal of cardiovascular drugs : drugs, devices, and other interventions     Volume:  9     ISSN:  1175-3277     ISO Abbreviation:  Am J Cardiovasc Drugs     Publication Date:  2009  
Date Detail:
Created Date:  2009-05-25     Completed Date:  2009-08-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100967755     Medline TA:  Am J Cardiovasc Drugs     Country:  New Zealand    
Other Details:
Languages:  eng     Pagination:  177-96     Citation Subset:  IM    
Affiliation:
Department of Pathology, Toronto General Hospital/University Health Network, Toronto, Ontario, Canada.
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MeSH Terms
Descriptor/Qualifier:
Arrhythmias, Cardiac / chemically induced,  drug therapy
Cardiovascular Agents / therapeutic use*
Cardiovascular Diseases / chemically induced*,  pathology,  physiopathology
Clinical Trials as Topic
Cocaine / adverse effects*,  analysis,  pharmacology
Death, Sudden, Cardiac / etiology,  prevention & control
Heart / drug effects,  physiopathology
Heart Failure / chemically induced,  drug therapy
Humans
Myocardial Infarction / chemically induced,  drug therapy
Myocardium / pathology
Practice Guidelines as Topic
Chemical
Reg. No./Substance:
0/Cardiovascular Agents; 50-36-2/Cocaine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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