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

Abstract

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.

Ventricular tachycardia revealing drug abuse induced myocarditis: two case reports

“…In fact, complete right bundle branch block, shown in our case, was described to be the consequence of sodium channel blockade, the main mechanism of action of cocaine 5. In contrast, for the second patient, cannabis is likely the responsible drug because of the occasional consumption of cocaine compared to daily use of cannabis, in addition to the absence of cocaine‐related ECG signs 7.…”

“…Moreover, catecholamine excess induced by cocaine or cannabis intoxication can also be evocated as VT trigger on such a vulnerable myocardium 5, 6.…”

Drug Abuse-Induced Cardiac Arrhythmias: Mechanisms and Management

“…In fact, early and minimal toxicity results in the impairment of conduction on the right side leading to a rightward axis deviation and QRS duration prolongation, and then, as toxicity increases, a right bundle branch block (RBBB) appears in the precordial leads (Figure 1). This pattern associated with sinus tachycardia, often shown in case of cocaine intoxication, may be confused with a true ventricular tachycardia resulting from a reentry or focal mechanism that can also complicate cocaine intoxication as reported in many series [4,9,10].…”

“…Four mechanisms are implicated in the genesis of arrhythmia in case of cocaine intoxication: sodium channel blockade, potassium channel blockade, catecholamine excess, and finally myocardial infarction (MI) and myocarditis [4]. Recently, sinus bradycardia has been described as a result of chronic cocaine use [5][6][7] that may be related to a cocaine-induced desensitization of beta-adrenergic receptors [6].…”

Using Journal Review Articles to Increase the Dissemination of Keynote and Symposia Lectures at International Medical Congresses

“…The symposium started with discussion of the epidemiology of cocaine use and toxicity, followed by overview of the impact of cocaine on sodium and other myocardial ion channels and finished with a pragmatic clinical overview of the presentation and management of cocaine-related arrhythmias. Following discussion with the British Journal of Clinical Pharmacology, the journal of the Clinical Section of the BPS, it was agreed, prior to the symposium, that they would publish a series of review articles from the symposium in a single future issue of the journal [1][2][3]. These articles underwent the usual peer-review process prior to publication, and the series of review articles were published in the print version of the journal approximately 1 year after the symposium.…”