Accelerated Ventricular Rhythm and Cocaine Abuse

Benchimol, Alberto; Bartall, Haim; Desser, Kenneth B.

doi:10.7326/0003-4819-88-4-519

Cited by 146 publications

(22 citation statements)

References 4 publications

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“…Cocaine used as a local anesthetic agent during laryngoscopy has been observed to increase the frequency of premature ventricular complexes.37 A few isolated cases of ventricular tachycardia and fibrillation associated with cocaine use have been reported?. 38,39 but pmarrhythrmc fatalities of cocaine are not likely to be identified clinically. Mittleman and Welti22 reported 24 cases of sudden death among cocaine abusers.…”

Section: Cocaine-induced Proarrhythmia and Cardiac Arrestmentioning

confidence: 99%

Cardiac complications of cocaine abuse

Chakko

Myerburg

1995

Clinical Cardiology

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Summary: Cardiac complications of cocaine abuse and a rational approach to evaluating and managing them are described. Cardiac abnormalities reported among asymptomatic cocaine abusers include echocardiographic left ventricular hypertrophy and segmental wall motion abnormalities. Electrocardiogram may reveal increased QRS voltage, ST-T changes, and pathologic Q waves. Episodes of ST elevation may be seen during Holter monitoring. The management of cocaine-abusing patients who present to an emergency room with acute chest pain is controversial because the two reported studies yielded conflicting results regarding the incidence of myocardial infarction (MI). Even in the absence of infarction, electrocardiographic abnormalities are common among these patients, which complicates the decision-malung regarding hospitalization. Pathophysiology of cocaine-related MI is discussed. Distinct clinical features of cocaine-related MI make it clear that the association between the two is not just temporal. However, considering the number of persons abusing cocaine, it is a rarity. Beta-adrenergic blockers should be avoided in the treatment of cocaine-induced myocardial ischemia which is best treated with nitrates and calcium-channel blockers. Reports of cocaineinduced myocarditis and cardiomyopathy are reviewed. Experimental studies and clinical case reports suggest that cocaine may cause lethal arrhythmias. Cocaine prolongs repolarization by a depressant effect on potassium current and may generate early aferdepolarizations. It is possible that cocaine-associated arrhythmias are secondary to vasospasm-related ischemia and reperfuoion as well.

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Section: Cocaine-induced Proarrhythmia and Cardiac Arrestmentioning

confidence: 99%

Cardiac complications of cocaine abuse

Chakko

Myerburg

1995

Clinical Cardiology

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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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“…Numerous acute medical problems have been associated with cocaine abuse, including cardiac dysrhythmias [2][3][4][5][6][7]. Although the etiology of cocaine-associated dysrhythmias is complex and not fully understood, lethal ventricular dysrhythmias are a theorized cause of sudden death associated with cocaine use [8].…”

Section: Introductionmentioning

confidence: 99%

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity

et al. 2005

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Introduction: Cocaine is a common drug of abuse and use has been associated with ventricular dysrhythmias. Published guidelines suggest that amiodarone is the first line antidysrhythmic for ventricular tachycardia and fibrillation. However, the effects amiodarone in the setting of cocaine toxicity are unknown and unstudied. The purpose of this study was to evaluate the safety and efficacy of amiodarone pretreatment in a murine model of acute cocaine toxicity.Methods: This was a randomized, blinded, placebo controlled investigation using male CF-1 mice weighing 29-37 g. First, the safety of an intraperitoneal dose of amiodarone (40 mg/kg) was confirmed in 5 mice. Second, based on preliminary investigations, an approximate intraperitoneal LD 50 dose of cocaine (110 mg/kg) was identified and used as the cocaine dose in this study. Animals were then randomized to 2 groups. The control group received 0.5 mL of intraperitoneal 0.9% saline 30 minutes before cocaine. The study group received 40 mg/kg of intraperitoneal amiodarone (40 mg/kg) 30 minutes before cocaine. A blinded observer monitored mice for 2 hours after cocaine administration.Results: No mice in the amiodarone-only group developed any signs of toxicity or died. In the saline ϩ cocaine group 31/32 (96.9%; 95% CI 83.8 to 99.9) mice seized with a median time to seizure of 2.5 minutes, and 23/32 (71.9%; 95% CI 52.3 to 86.3) died with a median time to death of 5.5 minutes. In the amiodarone ϩ cocaine group 31/33 (93.9%; 95% CI 79.0 to 99.3) mice seized with a median time to seizure of 2.0 minutes, and 24/33 (72.7%; 95% CI 54.5 to 86.7) died with a median time to death of 6.0 minutes. All animals that died did so within 9 minutes. The difference in the proportion of animals dying in the amiodarone ϩ cocaine group compared to the saline ϩ cocaine group was 0.008 (Ϫ21 to 22%).Conclusions: In this study, pretreatment with amiodarone in cocaine poisoned mice resulted in no change in seizure incidence or mortality. However, definite conclusions about the reason for these findings cannot be drawn from this model.

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Accelerated Ventricular Rhythm and Cocaine Abuse

Cited by 146 publications

References 4 publications

Cardiac complications of cocaine abuse

Cardiac complications of cocaine abuse

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

The effect of amiodarone pretreatment on survival of mice with cocaine toxicity

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