14th International Congress
THE "NEW FRONTIERS"
OF ARRHYTHMIAS 2000

Jan. 29 - Feb. 5, 2000
Marilleva, Trento, Italy

RT-149

Acquired QT syndrome. The mechanistic background

Wilhelm Haverkamp, Paulus Kirchhof, Lars Eckardt, Gerold Mönnig, Martin Borggrefe, Günter Breithardt.
Hospitalof the Westfälische Wilhelms-University, Department of Cardiology and Angiology and Institute for Arteriosclerosis Research, Münster, Germany

Introduction

The long QT syndrome (LQTS) is either an inherited or an acquired disorder, characterized primarily by prolongation of the QT interval, by recurrent torsade de pointes (TDP)-related syncope, and sudden cardiac death. The congenital variant has recently been identified as a genetic channelopathy. TDP secondary to acquired abnormal QT prolongation has been described under a variety of circumstances. The most common cause of the arrhythmia seems to be the administration of antiarrhythmic drugs that prolong the action potential, i.e. class IA and class III agents^1,2. The incidence of TDP in patients treated with quinidine has been estimated to range between 2.0 and 8.8% . The incidence of TDP associated with sotalol which besides its class III activity possesses significant beta-blocking activity has been estimated to range between 1.8 and 4.8%. TDP secondary to exposure to newer so-called “pure” class III agents (e.g. dofetilide, d-sotalol, almokalant, ibutilide), and treatment with N-acetyl-procainamide, the major metabolite of procainamide, has been well documented. As with other drugs known to prolong myocardial repolarization, the incidence of TDP is dose-dependent, i.e. it increases with higher dosages/drug concentrations.

TDP have not only been reported to occur secondary to treatment with cardiac or antiarrhythmic drugs, but also during treatment with several other drugs not generally thought to have significant effects on myocardial repolarization (e.g. phenothiazines, antidepressants, other psychotropic drugs, antihistamines of the H1 blocking type, the promotility agent cisapride, and some antibiotics, most notably erythromycin). Estimation of the incidence of TDP during treatment with non-cardiovascular drugs is difficult. A large number of reported case reports and individual small series suggest that the occurrence of this particular form of drug-related proarrhythmia is not a trivial problem.

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