Recent advances in understanding the mechanisms of drug-induced torsades de pointes arrhythmias

• Published in: The American journal of cardiology Vol. 64; no. 20; pp. J29 - J32
• Main Authors: Sasyniuk, Betty I., Valois, Maria, Toy, William
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 05-12-1989; Elsevier
• Subjects: Anti-Arrhythmia Agents - adverse effects; Biological and medical sciences; Biomechanical Phenomena; Drug toxicity and drugs side effects treatment; Electrophysiology; Heart - drug effects; Heart - physiology; Humans; Medical sciences; Pharmacology. Drug treatments; Tachycardia - chemically induced; Toxicity: cardiovascular system; Heart; Treatment; Arrhythmia; Toxicity; Cardiovascular disease; Complication; Antiarrhythmia agent; Excitability disorder
• ISSN: 0002-9149; 1879-1913
• DOI: 10.1016/0002-9149(89)91194-6

QTU prolongation and polymorphic ventricular rachycardia “torsades de pointes” have occurred in association with electrolyte abnormalities and during therapy with class IA and III antiarrhythmic drugs. Several recent studies have suggested that the arrhythmia may be due to bradycardia-dependent early afterdepolarirations and triggered activity. These drugs produce 2 types of triggered activity, each with a different frequency profile. The possible role of each type in arrhythmia generation is discussed. The existing evidence suggests that drug-induced triggered activity may originate in the Purkinje system. Triggered activity can be abolished or prevented by various interventions that are also effective clinically. The results of studies at the cellular level, when compared with recordings of monophasic action potentials in vivo, suggest a role for early afterdepolarizations in torsades de pointes arrhythmins.