Highlights the potential for fatal proarrhythmic effects of flecainide in patients with WPW syndrome and atrial fibrillation, even with structurally normal hearts.
The Wolff-Parkinson-White syndrome can be complicated by atrial fibrillation that may increase morbidity and mortality. Different pharmacologic therapy, includes class IA, IC, and III agents, has been used in such cases with variable success. We now use less pharmacologic intervention with development of an electrode catheter ablation for accessory pathways. However, antiarrhythmic agents are still being used, especially when an electrode catheter ablation is unavailable or if a patient refuses such a procedure. Therefore, it is prudent that one understands each antiarrhythmic agents' electropharmacologic properties as well as its potential proarrhythmic effect in order to accurately assess each drug's risk-benefit ratio. We present a case that illustrates electropharmacologic properties of quinidine, flecainide, sotalol, and amiodarone on various cardiac tissues, as well as possible proarrhythmic effect of flecainide on a structurally normal heart.
Chun et al. (Mon,) studied this question.
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