Electrophysiologic effects of flecainide acetate on sinus node function, anomalous atrioventricular connections, and pacemaker thresholds

The acute electrophysiologic effects of i.v. flecainide acetate (2 mg/kg body weight) were assessed in 71 patients undergoing electrophysiologic study. Ten patients underwent investigation for sinus node dysfunction. Sinus cycle length shortened slightly, from 980 ± 292 to 931 ± 276 ms (p < 0.01). Un-corrected or corrected sinus node recovery times or sinoatrial conduction time (according to the methods of Strauss and Narula) did not change in 6 patients with normal sinus node function and in 3 of 4 patients with abnormal sinus node function at rest. In the remaining patient maximal sinus node recovery time increased from a value at rest of 5,185 ms to 23,460 ms after flecainide. In the same patient sinoatrial conduction times at rest increased from 159 ms (Strauss method) and 143 ms (Narula method) to 1,398 and 1,455 ms, respectively, after flecainide. Thirty-three patients underwent electrophysiologic evaluation of anomalous atrioventricular (AV) pathways and reentrant tachycardias. Flecainide significantly prolonged accessory AV pathway anterograde and retrograde refractoriness. Anterograde accessory pathway block occurred in 33% of patients and retrograde accessory pathway block in 44%. Flecainide was successful in the acute termination of 86% of orthodromic atrioventricular reentrant tachycardias. In 15 patients with dual AV nodal pathways, only retrograde “fast” AH pathway refractoriness was significantly increased by flecainide, which was successful in the acute termination of 88% of intra-AV nodal reentrant tachycardias. In 28 patients who underwent endocardial pacing threshold assessment before and after i.v. flecainide, the acute threshold rose by a maximum of 117%, whereas the chronic threshold rose by a maximum of 83%. In 5 of these patients, oral flecainide increased chronic endocardial pacing threshold, in a dose-related manner, by as much as 200%.