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When is QT prolongation antiarrhythmic and when is it proarrhythmic?

1989; Elsevier BV; Volume: 63; Issue: 12 Linguagem: Inglês

10.1016/0002-9149(89)90059-3

1879-1913

Bramah N. Singh,

Cardiac Arrhythmias and Treatments

A large number of pathophysiologic conditions and pharmacologic interventions produce a significant lengthening of the QT interval. For many physicians a long QT interval continues to be associated with a propensity for polymorphic ventricular tachycardia to develop.’ This belief undoubtedly stems from an appreciation of the life-threatening arrhythmic complications of the congenital forms of the long QT-interval syndromes.2 The fear of an arrhythmogenic correlate of prolonged QT interval became entrenched in the early 1960s (about the time potent oral diuretics began to be introduced) when it was recognized that “quinidine syncope” was due to paroxysmal ventricular arrhythmia.3 This arrhythmia was called torsades de pointes.4 The features of this electrocardiographic and clinical entity are now clearly delineated.5 It occurs in the setting of long QT interval, and most cases are drug induced. The tendency for torsades de pointes to develop in the setting of prolonged QT interval is now known to be aggravated by the presence of bradycardia and severe electrolyte disturbances, especially hypokalemia.6 In recent years, a number of observations on the clinical significance of drug-induced lengthening of the QT interval have been made.7 First, we now know that there is not a linear relation between the degree of lengthening of the QT interval and the development of torsades de pointes. For example, a modest lengthening of the QT interval with quinidine may lead to the development of torsades de pointes, whereas with a profound increase, as with amiodarone, it rarely occurs. Second, for a given degree of QT lengthening produced by a variety of drugs, the incidence of torsades de pointes varies from one compound to the next. Third, there are several instances of QT prolongation in clinical situations (e.g., hypocalcemia and hypothyroidism) in which’ torsades de pointes or any other form of tachyarrhythmias is exceedingly uncommon. Finally, there is now compelling evidence7 that the lengthening of the QT interval induced by a number of cardioactive compounds (e.g., amiodarone, sotalol) constitutes a discrete antiarrhythmic and antifibrillatory mechanism as suggested 19 years ago. 8,g How does one reconcile these 2 seem-