Flecainide depressed anterograde and retrograde conduction of the accessory pathway and terminated circus movement tachycardia in 8 of 9 patients with Wolff-Parkinson-White syndrome.
Observational (n=12)
Does flecainide alter the electrophysiological properties of accessory pathways in patients with Wolff-Parkinson-White syndrome?
Flecainide depresses conduction in accessory pathways and may be beneficial for treating paroxysmal supraventricular tachycardias in patients with Wolff-Parkinson-White syndrome.
The effect of flecainide in 12 patients with the Wolff-Parkinson-White syndrome was analyzed with respect to the anterograde and retrograde conduction properties of the accessory pathway, the modes of initiation and termination of circus movement tachycardias, and the ventricular response during induced atrial fibrillation. The principal effect of this drug was to depress both anterograde and retrograde conduction of the accessory pathway. In 8/9 cases circus movement tachycardia was terminated by prolongation of the retrograde effective refractory period of the accessory pathway. Flecainide increased the shortest and the mean cycle length during induced atrial fibrillation. It is concluded that the drug may be of potential benefit in patients with paroxysmal supraventricular tachycardias in patients with the Wolff-Parkinson-White syndrome.
Neuß et al. (Sun,) conducted a observational in Wolff-Parkinson-White syndrome (n=12). Flecainide was evaluated on Electrophysiological properties of the accessory pathway, initiation/termination of circus movement tachycardias, and ventricular response during induced atrial fibrillation. Flecainide depressed anterograde and retrograde conduction of the accessory pathway and terminated circus movement tachycardia in 8 of 9 patients with Wolff-Parkinson-White syndrome.