Clinical efficacy and electrophysiologic effects of encainide in patients with Wolff-Parkinson-White syndrome.

Abstract

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 was 328 ± 66 msec in patients in whom antegrade conduction block occurred, and it was 247 + 21 msec (p < .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 < .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 43.8 to 238.3 ± 87.9 msec (p < .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. Circulation 69, No. 2, 278-287, 1984. SUPRAVENTRICULAR TACHYCARDIA frequently occurs in patients who have accessory atrioventricular (AV) pathways. Reentrant tachycardia most commonly conducts antegradely over the normal AV pathway and retrogradely over the accessory pathway.

Electropharmacology of sotalol in patients with Wolff-Parkinson-White syndrome.

“…12, 13. 16, 35, 44-49 The agents that appear to be most potent in this setting are those that combine AV nodal and accessory connection effects.6 49 Such effects have been shown with intravenous sotalol23, 26,27 and with low, fixed dosages of oral sotalol.28 The present investigation examines the contributions of /3-adrenoceptor blockade and class III effects to the antiarrhythmic efficacy of oral sotalol in WPW syndrome. Induction of sustained reciprocating tachycardia was prevented at ,3-adrenoceptor-blocking dosages in 55% of patients.…”

Effects of flecainide on ectopic atrial automaticity and conduction.

“…Flecainide-induced changes in the amplitude-excitability relationship may also explain its efficacy in suppressing accessory pathway conduction. [5][6][7]17,18 In this case, it may be hypothesized that a reduction in excitability of a large tissue mass connected to a smaller accessory pathway increases the "load" on impulses conducting through the latter. Moreover, under conditions in which regenerative inward Na+ current is also reduced,2122 it would be expected that the current generated by accessory pathway fibers would be a less efficacious stimulus for the activation of resting fibers, resulting in conduction failure.…”

Encainide

“…Prystowsky et al [61] examined encainide (mean daily dose 197 mg) in 19 patients who had recurrent AV reentrant tachycardia for a mean of 15.8 years and had failed an average of 3.6 antiarrhythmics. Encainide caused complete conduction block in patients with anterograde and retrograde accessory pathways in 50~: of the patients tested.…”