Encainide prevented induction of tachycardia in 10 of 19 patients with Wolff-Parkinson-White syndrome and increased tachycardia cycle length from 313.9 to 418.3 msec in the rest (P<0.001).
Does encainide alter electrophysiologic properties and prevent recurrent tachycardia in patients with Wolff-Parkinson-White syndrome?
Encainide effectively alters the electrophysiologic properties of accessory pathways and prevents the recurrence of atrioventricular reentrant tachycardia in patients with Wolff-Parkinson-White syndrome.
Tasa de eventos absoluta: 418.3% vs 313.9%
valor p: p=<0.001
We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.
Prystowsky et al. (Wed,) conducted a other in Wolff-Parkinson-White syndrome (n=19). Encainide vs. Baseline (before therapy) was evaluated on Cycle length of tachycardia in patients with inducible tachycardia (p=<0.001). Encainide prevented induction of tachycardia in 10 of 19 patients with Wolff-Parkinson-White syndrome and increased tachycardia cycle length from 313.9 to 418.3 msec in the rest (P<0.001).