Acute Cardiac Events Temporally Related to Cocaine Abuse

Isner, Jeffrey M.; Estes, N.A. Mark; Thompson, Paul D.; Costanzo-Nordin, Maria Rosa; Subramanian, Ramiah; Miller, Gary; Katsas, George G.; Sweeney, Kristin G.; Sturner, William Q.

doi:10.1056/nejm198612043152302

Cited by 573 publications

(102 citation statements)

References 22 publications

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“…Multiple reports and case series describe patients who develop myocardial infarction in close temporal association with cocaine use; only a few are cited for the reader to review [6,7,48,64]. In all of these series and additional individual case reports some patients developed ventricular tachycardia, ventricular fibrillation, and torsades de pointes.…”

Section: Ischaemia and Infarctionmentioning

confidence: 99%

Treatment of patients with cocaine‐induced arrhythmias: bringing the bench to the bedside

Hoffman

2010

Brit J Clinical Pharma

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Widespread use of cocaine and its attendant toxicity has produced a wealth of benchwork studies and small animal investigations that evaluated the effects of cocaine on the cardiovascular system. Despite this wealth of knowledge, very little is known about the frequency or types of arrhythmias in patients with significant cocaine toxicity. The likely aetiologies; catecholamine excess, sodium channel blockade, potassium channel blockade, calcium channel effects, or ischaemia may act alone or in concert to produce a vast array of clinical findings that are modulated by hyperthermia, acidosis, hypoxia and electrolyte abnormalities. The initial paper in the series by Wood & Dargan providing the epidemiological framework of cocaine use and abuse is followed by a detailed review of the electrophysiological effects of cocaine by O'Leary & Hancox. This review is designed to complement the previous papers and focuses on the diagnosis and treatment of patients with cocaine‐associated arrhythmias.

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Section: Ischaemia and Infarctionmentioning

confidence: 99%

Treatment of patients with cocaine‐induced arrhythmias: bringing the bench to the bedside

Hoffman

2010

Brit J Clinical Pharma

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“…The effects of cocaine on the heart have been popularized by the sudden deaths of sports figures who used the drug and a series of case studies showing a temporal relation between the use of cocaine and cardiac illness. [1][2][3][4][5][6][7][8] Although there had been widespread belief among users that cocaine is safe and nonaddicting, it is now clear that its cardiotoxic effects in any given individual are unpredictable.…”

Section: U Clinical Progress Seriesmentioning

confidence: 99%

The effects of acute and chronic cocaine use on the heart.

et al. 1992

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It is clear that cocaine has cardiotoxic effects. Acute doses of cocaine suppress myocardial contractility, reduce coronary caliber and coronary blood flow, induce electrical abnormalities in the heart, and in conscious preparations increase heart rate and blood pressure. These effects will decrease myocardial oxygen supply and may increase demand (if heart rate and blood pressure rise). Thus, myocardial ischemia and/or infarction may occur, the latter leading to large areas of confluent necrosis. Increased platelet aggregability may contribute to ischemia and/or infarction. Young patients who present with acute myocardial infarction, especially without other risk factors, should be questioned regarding use of cocaine. As recently pointed out by Cregler, cocaine is a new and sometimes unrecognized risk factor for heart disease. Acute depression of LV function by cocaine may lead to the presence of a transient cardiomyopathic presentation. Chronic cocaine use can lead to the above problems as well as to acceleration of atherosclerosis. Direct toxic effects on the myocardium have been suggested, including scattered foci of myocyte necrosis (and in some but not all studies, contraction band necrosis), myocarditis, and foci of myocyte fibrosis. These abnormalities may lead to cases of cardiomyopathy. Left ventricular hypertrophy associated with chronic cocaine recently has been described. Arrhythmias and sudden death may be observed in acute or chronic use of cocaine. Miscellaneous cardiovascular abnormalities include ruptured aorta and endocarditis. Most of the cardiac toxicity with cocaine can be traced to two basic mechanisms: one is its ability to block sodium channels, leading to a local anesthetic or membrane-stabilizing effect; the second is its ability to block reuptake of catecholamines in the presynaptic neurons in the central and peripheral nervous system, resulting in increased sympathetic output and increased catecholamines. Other potential mechanisms of cocaine cardiotoxicity include a possible direct calcium effect leading to contraction of vessels and contraction bands in myocytes, hypersensitivity, and increased platelet aggregation (which may be related to increased catecholamine). The correct therapy for cocaine cardiotoxicity is not known. Calcium blockers, alpha-blockers, nitrates, and thrombolytic therapy show some promise for acute toxicity. Beta-Blockade is controversial and may worsen coronary blood flow. In patients who develop cardiomyopathy, the usual therapy for this entity is appropriate.

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“…Antipsychotic agents such as clozapine (11), but not droperidol (12), are rarely associated with cardiomyopathy and myocarditis. Urine drug immunoassay did not detect any sympathomimetic amines well known to cause cardiovascular sequelae (13). There are no reports of an association between maintenance methadone dosing and cardiomyopathy.…”

Section: To the Editormentioning

confidence: 89%