Amiodarone Therapy After Previous Sotalol-induced Torsade de Pointes: Analysis of QT Dispersion to Predict Proarrhythmia

Abstract

Background: Polymorphic ventricular tachycardia of the torsade de pointes type represents, potentially, the most dangerous side effect of antiarrhythmic drugs that prolong ventricular repolarization. Much effort has been devoted to the identification of the degree of drug-asso ciated QT prolongation that might predict the occurrence of torsade de pointes. However, there is still no general agreement as to which level of QT prolongation might be the harbinger of torsade and which may simply represent the manifestation of the class III antiarrhythmic effect of a given compound. Methods and Results: A 70-year-old woman who had survived an episode of cardiac arrest outside of a hospital was treated with dl-sotalol (320 mg/d). After 8 days of therapy, she devel oped two episodes of hemodynamically unstable torsade de pointes. Sotalol was withdrawn and after extensive diagnostic work, therapy with amiodarone was instituted. Despite the fact that the degree of QT prolongation observed during amiodarone therapy was comparable to that observed during sotalol exposure, the patient tolerated amiodarone and is now free of recurrent ventricular tachyarrhythmias over a follow-up period of I year. Analysis of QT dis persion in the surface electrocardiograph revealed a marked increase during sotalol therapy but not during amiodarone administration (77 vs 47 ms). During drug-free control, QT dis persion was 43 ms. Conclusions: These findings emphasize the potential usefulness of determination of QT dis persion from the surface ECG to assess disparity in ventricular recovery, which is known to favor the occurrence of torsade de pointes. These observations need to be corroborated in large prospective trials. Finally, this case report further emphasizes the low arrhythmogenic potential of amiodarone—an unexplained paradox, the understanding of which might provide insights for the development of newer antifibrillatory compounds.