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

QTU prolongation and polymorphic ventricular tachycardia "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 afterdepolarizations 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 suggest 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 arrhythmias.