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Evaluation and management of the cardiovascular complications of cocaine abuse

James P Morgan, MD, PhD
Section Editors
William J McKenna, MD
Stephen J Traub, MD
Deputy Editor
Brian C Downey, MD, FACC


Cocaine is among the most commonly used illicit recreational drugs worldwide. Because even casual use of cocaine may be associated with acute or chronic cardiovascular toxicity, the large numbers of exposed individuals represent a reservoir of patients who may present with sequelae related to the cardiovascular system. Thus, the cardiovascular history should include questions about cocaine use, specifically focusing on the occurrence of symptoms associated with ischemic heart disease.

Cocaine use is more frequently associated with acute rather than chronic cardiovascular illness. Among cocaine users who present to emergency departments, cardiovascular complaints, particularly chest pain, are common [1,2]. In such patients, acute coronary syndromes (including myocardial ischemia and infarction), aortic dissection and rupture, arrhythmias, myocarditis, and vasculitis need to be considered [3].

The cardiovascular effects and complications of cocaine use, as well as the management of cocaine-associated ischemia, will be reviewed here. Other issues relating to cocaine use, including the general approach to patients with chest pain and a history of cocaine use, are discussed elsewhere. (See "Cocaine use disorder in adults: Epidemiology, pharmacology, clinical manifestations, medical consequences, and diagnosis" and "Cocaine: Acute intoxication".)


The major cardiovascular effects of cocaine appear to be caused by the inhibition of norepinephrine reuptake into the synaptic cleft by sympathetic neurons [2]. Since reuptake is the major mechanism by which neurotransmitters are removed from active receptor sites, this inhibition results in potentiation of the response to sympathetic stimulation of innervated organs and to infused catecholamine. Cocaine may also enhance the release of catecholamines from central and peripheral stores [4,5]. The ensuing sympathomimetic actions (increased myocardial inotropy, heart rate, systemic blood pressure, and coronary artery constriction primarily at the capillary level) are mediated by stimulation of the alpha- and beta adrenergic receptors and result in increased myocardial oxygen demand and decreased myocardial perfusion. (See "Cocaine: Acute intoxication", section on 'Pharmacology'.)

Other cardiovascular effects of cocaine include promotion of thrombus formation (via activation of platelets, stimulation of platelet aggregability, and potentiation of thromboxane production) and proarrhythmia [6-8]. The cardiovascular effects produced by intravenous, intranasal, and inhaled cocaine are thought to be similar regardless of the route of ingestion. The clinical consequences of these effects are discussed below.


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