Frequency and type of electrocardiographic abnormalities in cocaine abusers (electrocardiogram in cocaine abuse)

Chakko, Simon; Sepúlveda, Sebastián; Kessler, Kenneth M.; Sotomayor, M.; Mash, Deborah C.; Prineas, Ronald J.; Myerburg, Robert J.

doi:10.1016/0002-9149(94)90315-8

Cited by 59 publications

(28 citation statements)

References 21 publications

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“…This typically produces supraventricular rhythms, most commonly sinus tachycardia but also re-entrant supraventricular tachycardia and atrial fibrillation. In the previously mentioned series of emergency department patients with acute cocaine toxicity sinus tachycardia was common, and supraventricular tachycardia was present in 5% [14]. Atrial fibrillation has only been noted in case reports and case series [48,49].…”

Section: Catecholamine Excess and Psychomotor Agitationmentioning

confidence: 97%

“…It is important to note that no study has systematically evaluated the electrocardiographic findings in a large group of patients with acute cocaine toxicity. A small study suggests that tachycardia is the most common finding, and that asymptomatic patients often have QRS prolongation, which may result from underlying heart disease [14]. In a few patients who have used cocaine a classic Brugada pattern has been noted [15][16][17].…”

Section: Sodium Channel Blockadementioning

confidence: 99%

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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: Catecholamine Excess and Psychomotor Agitationmentioning

confidence: 97%

Section: Sodium Channel Blockadementioning

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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“…3). In addition, several clinical reports [1][2][3][4][12][13][14]24 have documented that cocaine may lead to conduction disturbances, supraventricular and ventricular arrhythmias, and sudden death in the absence of myocardial ischemia or heart disease. Further supporting this premise, the proarrhythmic effects of sodium channel blocking drugs are well recognized, particularly in the presence of structural heart disease 25 .…”

Section: Discussionmentioning

confidence: 99%

“…Nevertheless, experimental studies evaluating cocaine's effects on programmed electrical stimulation-induced arrhythmias have had conflicting results, with cocaine either increasing or having a neutral effect on inducibility of ventricular arrhythmias 6,[8][9][10][11] . Further, although supraventricular tachyarrhythmias, including atrial tachycardia, atrial flutter, and atrial fibrillation, can also occur in the setting of cocaine abuse 1,3,[12][13][14] , limited data are is available assessing the impact of the drug on inducibility of atrial arrhythmias.Therefore, we sought to characterize the actions of high plasma concentrations of cocaine on atrial and ventricular electrophysiology and arrhythmia inducibility in a canine preparation with normal hearts. …”

mentioning

confidence: 99%

Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts

Fenelon¹,

Uchôa²,

Otobone³

et al. 2003

Arq. Bras. Cardiol.

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Cocaine abuse has markedly increased over the past decade having reached epidemic levels in Western countries [1][2][3][4] . Cocaine intoxication is associated with a significant morbidity and mortality and is a frequent cause of drug-related sudden death 2,3 . Most evidence suggests that cocaineinduced sudden death results from its cardiovascular consequences, particularly ventricular arrhythmias 1 . However, the mechanisms involved in the genesis of these arrhythmias remain incompletely understood. Although cocaineinduced arrhythmias may be associated with myocardial ischemia or infarction 3,5 , cocaine may be arrhythmogenic in the absence of an ischemic event 1 . In addition to its powerful indirect sympathomimetic actions 1-4 (promoted by blockade of presynaptic reuptake of norepinephrine and dopamine), high doses of cocaine exert significant local anesthetic effects that could promote conduction disturbances and reentrant arrhythmias 1,3,6,7 . Nevertheless, experimental studies evaluating cocaine's effects on programmed electrical stimulation-induced arrhythmias have had conflicting results, with cocaine either increasing or having a neutral effect on inducibility of ventricular arrhythmias 6,[8][9][10][11] . Further, although supraventricular tachyarrhythmias, including atrial tachycardia, atrial flutter, and atrial fibrillation, can also occur in the setting of cocaine abuse 1,3,[12][13][14] , limited data are is available assessing the impact of the drug on inducibility of atrial arrhythmias.Therefore, we sought to characterize the actions of high plasma concentrations of cocaine on atrial and ventricular electrophysiology and arrhythmia inducibility in a canine preparation with normal hearts. MethodsBeagle dogs (n=12; weight, 9-13 kg) were divided into 2 groups: cocaine (n=8) and sham control (n=4). The study protocol was approved by the research committee of the Objective -To characterize the cardiac electrophysiologic effects of cocaine. Methods -In 8 dogs (9-13 kg), electrophysiologic parameters and programmed stimulation were undertaken using transvenous catheters at baseline, and after cocaine intravenous infusion (12 mg/kg bolus followed by 0.22 mg/ kg/min for 25 minutes).Results -Cocaine plasma levels (n=5) rose to 6.73± 0.56 µg/mL. Cocaine did not affect sinus cycle length and arterial pressure. Cocaine prolonged P wave duration (54±6 vs 73±4 ms, P<0.001), PR interval (115±17 vs 164±15 ms, P<0.001), QRS duration (62±10 vs 88±14 ms, P<0.001), and QTc interval (344±28 vs 403±62 ms, P=0.03) but not JT interval (193±35 vs 226±53 ms, NS). Cocaine prolonged PA (9±6 vs 23±8 ms, P<0.001), AH (73±16 vs 92±15 ms; P=0.03), and HV (35±5 vs 45±3ms; P<0.001) intervals and Wenckebach point (247±26 vs 280±28 ms, P=0.04). An increase occurred in atrial (138±8 vs 184± 20 ms; P<0.001) and ventricular (160±15 vs 187±25 ms; P=0.03)

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“…Cocaine can also result in cardioembolism due to its cardiotoxic effects, including myocardial infarction and cardiomyopathy [10]. Cocaine blocks potassium channels, resulting in prolongation of action potential duration (APD) and QT interval [11,12]. Cocaine toxicity has been associated with different cardiac arrhythmias, including torsades, but the combination of cocaine and ethanol is considered to be more arrhythmogenic than either substance alone [13,14].…”

mentioning

confidence: 99%

Neurotoxic and cardiotoxic effects of cocaine and ethanol

2009

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Introduction: Concurrent abuse of alcohol and cocaine results in the formation of cocaethylene, a powerful cocaine metabolite. Cocaethylene potentiates the direct cardiotoxic and indirect neurotoxic effects of cocaine or alcohol alone.Case Report: A 44-year-old female with history of cocaine and alcohol abuse presented with massive stroke in the emergency department. CT scan revealed extensive left internal carotid artery dissection extending into the left middle and anterior cerebral arteries resulting in a massive left hemispheric infarct, requiring urgent decompressive craniectomy. The patient had a stormy hospital course with multiple episodes of torsades de pointes in the first 4 days requiring aggressive management. She survived all events and was discharged to a nursing home with residual right hemiplegia and aphasia.Conclusion: The combination of ethanol and cocaine has been associated with a significant increase in the incidence of neurological and cardiac emergencies including cerebral infarction, intracranial hemorrhage, myocardial infarction, cardiomyopathy, and cardiac arrhythmias. The alteration of cocaine pharmacokinetics and the formation of cocaethylene have been implicated, at least partially, in the increased toxicity of this drug combination.

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Frequency and type of electrocardiographic abnormalities in cocaine abusers (electrocardiogram in cocaine abuse)

Cited by 59 publications

References 21 publications

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

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

Characterization of the in vivo cardiac electrophysiologic effects of high-dose cocaine in closed-chest, anesthetized dogs with normal hearts

Neurotoxic and cardiotoxic effects of cocaine and ethanol

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