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Updated: Jul 26, 2026

Determination of the Relative Cell Surface and Total Expression of Recombinant Ion Channels Using Flow Cytometry
Published on: September 28, 2016
Cocaine-induced channelopathies: emerging evidence on the multiple mechanisms of sudden death
Jerry L Bauman1, Robert J DiDomenico
1University of Illinois at Chicago, Department of Pharmacy Practice, Section of Cardiology 60612, USA.
Abstract:
Sudden death due to cocaine in the absence of myocardial infarction has been attributed to the precipitation of life-threatening arrhythmias not unlike that due to antiarrhythmic drugs. Cocaine is a slow on-off sodium blocker and a fast on-off potassium blocker. Effects on repolarization are biphasic: At low concentrations, cocaine delays ventricular recovery, whereas at higher levels, cocaine hastens it. Two distinct clinical profiles emerge from case reports of electrocardiographically documented life-threatening arrhythmias attributed to cocaine. The first is monomorphic slow ventricular tachycardia or idioventricular rhythm that occurs in overdose situations and appears to reflect excessive sodium channel block; it may respond to sodium bicarbonate. The second is torsade de pointes that occurs in recreational users who have underlying risks for this tachycardia (such as fully or partially expressed congenital long QT syndrome) and reflects potassium channel blockade. These clinical observations can be explained by recent findings regarding the electrophysiologic effects of cocaine. Other patterns of severe arrhythmias due to cocaine may yet emerge.
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