Cardiac complications of cocaine abuse

Chakko, Simon; Myerburg, Robert J.

doi:10.1002/clc.4960180206

Cited by 60 publications

(30 citation statements)

References 34 publications

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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%

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confidence: 99%

“…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][2][3][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] .…”

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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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Section: Discussionmentioning

confidence: 99%

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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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“…Chronic cocaine use in young men who were normotensive and had no symptoms or signs of heart diseases had electrocardiographic and echocardiographic abnormalities including LV hypertrophy (54%), LVEF Ͻ0.45 (4%), increased QRS voltage (23%), and episodes of ST-segment elevation on ambulatory monitoring (33%) (Chakko and Myerburg, 1995). However, the mechanism whereby chronic cocaine use predisposes to myocardial injury remains incompletely understood.…”

Section: Introductionmentioning

confidence: 99%

“…There have been increasing numbers of reports of dilated cardiomyopathy in cocaine abusers. Wiener et al (1986) were the first to describe the occurrence of DCM in the absence of atherosclerotic coronary artery disease in two patients who were cocaine abusers.Chronic cocaine use in young men who were normotensive and had no symptoms or signs of heart diseases had electrocardiographic and echocardiographic abnormalities including LV hypertrophy (54%), LVEF Ͻ0.45 (4%), increased QRS voltage (23%), and episodes of ST-segment elevation on ambulatory monitoring (33%) (Chakko and Myerburg, 1995). However, the mechanism whereby chronic cocaine use predisposes to myocardial injury remains incompletely understood.…”

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Chronic Exposure to Cocaine Binging Predisposes to an Accelerated Course of Dilated Cardiomyopathy in Conscious Dogs following Rapid Ventricular Pacing

Parikh

Nikolaidis²,

Stolarski³

et al. 2005

J Pharmacol Exp Ther

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Despite extensive study, the extent to which cocaine use predisposes to cardiac injury remains unknown. We hypothesized that chronic cocaine binging would increase susceptibility to a subsequent cardiac insult, even in the absence of demonstrable effects on baseline hemodynamics. We studied progression of dilated cardiomyopathy (DCM) induced by rapid ventricular pacing (240 beats per minute) in five conscious, chronically instrumented dogs, after exposure to repetitive cocaine binging (COC) in the form of four consecutive 1 mg/kg i.v. boluses daily for 8 days, to simulate human cocaine abuse. We compared the results with nine control dogs (CON) undergoing the exact pacing protocol, without prior cocaine exposure. Baseline hemodynamics were not significantly altered by chronic cocaine exposure. Following 2 weeks of pacing, COC dogs exhibited accelerated progression to DCM, depressed plasma nitric oxide levels (CON, 17 Ϯ 2 M; COC, 10 Ϯ 2 M, p Ͻ 0.05), and a significantly greater increase in plasma epinephrine (CON, 33 Ϯ 6 pg/ml; COC, 104 Ϯ 24 pg/ml). After only 2 weeks of pacing, COC dogs demonstrated progressive DCM of a magnitude comparable with end-stage pacing-induced DCM. Chronic cocaine binging increases susceptibility to a subsequent myocardial insult and accelerates progression of DCM in conscious dogs following rapid pacing. These data suggest that although chronic cocaine use alone may not affect myocardial function, it predisposes to greater susceptibility to a superimposed insult.Cocaine is responsible for the greatest number of hospitalizations in United States attributable to illicit drug use. According to a survey, it was reported that more than 25 million people had used cocaine at some time in their life, and 1.5 million were chronic users. The effects of cocaine on the cardiovascular system are multifaceted and remain incompletely understood. Cardiovascular manifestations of cocaine abuse include chest pain, myocardial ischemia and infarction, arrhythmias, infective endocarditis, aortic dissection and development of dilated cardiomyopathy, and heart failure (Wiener et al., 1986;Kloner et al., 1992;Mouhaffel et al., 1995). There have been increasing numbers of reports of dilated cardiomyopathy in cocaine abusers. Wiener et al. (1986) were the first to describe the occurrence of DCM in the absence of atherosclerotic coronary artery disease in two patients who were cocaine abusers.Chronic cocaine use in young men who were normotensive and had no symptoms or signs of heart diseases had electrocardiographic and echocardiographic abnormalities including LV hypertrophy (54%), LVEF Ͻ0.45 (4%), increased QRS voltage (23%), and episodes of ST-segment elevation on ambulatory monitoring (33%) (Chakko and Myerburg, 1995). However, the mechanism whereby chronic cocaine use predisposes to myocardial injury remains incompletely understood.There has been both confusion and controversy as to whether cocaine use predisposes to decreased myocardial contractility. Much of the evidence of cocaine-induced myoca...

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Effects of isradipine on intravenous cocaine-induced cardiovascular response: a pilot study

Johnson

Wells

Kenny

et al. 1999

Hum. Psychopharmacol. Clin. Exp.

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We examined the eects of isradipine, a dihydropyridine-class calcium channel antagonist, and eective antihypertensive medication on the pressor eects of cocaine on cardiac function. Using continuous non-invasive cardiovascular monitoring of heart rate, blood pressure, electrocardiographic recordings, and peripheral oxygen saturation, six healthy cocaine addicts received the following treatments in blinded, crossover fashion: (a) placebo; (b) intravenous cocaine (0 . 325 mg/kg iv), and (c) isradipine (10 mg pXoX cocaine. While cocaine-taking was associated with a small increase in blood pressure, this eect was not signi®cantly aected by isradipine. Isradipine pretreatment was, however, associated with a signi®cant re¯ex rise in heart rate following cocaine. Cocaine administration with or without isradipine produced no clinically signi®cant abnormalities of rhythm or conduction on the electrocardiogram and on peripheral oxygen saturation. While these results should be considered preliminary, they do suggest that this isradipine dose and/or dosing strategy does not have a clinically signi®cant cardioprotective eect during cocaine-taking.

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Cardiac complications of cocaine abuse

Cited by 60 publications

References 34 publications

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

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

Chronic Exposure to Cocaine Binging Predisposes to an Accelerated Course of Dilated Cardiomyopathy in Conscious Dogs following Rapid Ventricular Pacing

Effects of isradipine on intravenous cocaine-induced cardiovascular response: a pilot study

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