Flecainide in the Wolff-Parkinson-White syndrome.

The effects of flecainide on electrophysiologic parameters and arrhythmias in the Wolff-Parkinson-White syndrome were reviewed. Acute administration of flecainide blocks conduction across the accessory pathway in the anterograde direction in 40% and in the retrograde direction in 50% of cases and markedly prolongs refractoriness in the remaining cases. Flecainide has a lesser effect on refractoriness of the His-Purkinje system, atrium, ventricle, and atrioventricular node. Flecainide terminates atrioventricular tachycardia in greater than 80% of cases when given intravenously, and oral therapy prevents clinical recurrences in greater than 60% of cases, but may occasionally result in incessant tachycardia. Long-term efficacy is predicted by abolition of conduction across the accessory pathway or prevention of tachycardia induction at acute electrophysiologic testing. Concomitant administration of a beta-adrenoreceptor blocker results in greater long-term efficacy. Administered during preexcited atrial fibrillation, flecainide consistently slows the ventricular response and converts the majority of cases to sinus rhythm. Serious ventricular proarrhythmia is seen almost exclusively in patients with structural cardiac disease. Flecainide is a useful drug for the acute and chronic control of tachycardia in Wolff-Parkinson-White syndrome.