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  • Title: Electrophysiology of oral encainide.
    Author: Jackman WM, Zipes DP, Naccarelli GV, Rinkenberger RL, Heger JJ, Prystowsky EN.
    Journal: Am J Cardiol; 1982 Apr 01; 49(5):1270-8. PubMed ID: 6801954.
    Abstract:
    The electrophysiologic effects of oral encainide were assessed in 15 patients. Electrophysiologic studies were performed before and after 3 or more days of oral encainide therapy, 100 to 300 mg/day (mean 242 +/- 66). Patients received no other cardioactive drugs during this time. Encainide significantly (p less than 0.005) lengthened the following: A-H interval (74.5 +/- 21.5 to 105.5 +/- 39.1 ms, mean +/- standard deviation), the shortest atrial pacing cycle length maintaining 1:1 atrioventricular (A-V) nodal conduction (339.0 +/- 71.3 to 417.0 +/- 88.6 ms), H-V interval (47.5 +/- 7.8 to 67.1 +/- 12.9 ms), QRS interval (103.5 +/- 30.9 to 132.3 +/- 35.7 ms), right atrial (233.8 +/- 27.2 ms to 282.9 +/- 38.6 ms) and right ventricular (235.7 +/- 15.6 to 267.1 +/- 36.9 ms) effective refractory periods and Q-T interval (364.4 +/- 38.0 to 416.9 +/- 55.3 ms). The spontaneous sinus cycle length did not change significantly. In four patients who had accessory A-V muscle connections (two manifest, two concealed) encainide abolished anterograde conduction over the accessory pathway in two patients, and increased the retrograde effective refractory period and/or lengthened retrograde conduction time or blocked retrograde conduction in the accessory pathway, or all three variables, in all four patients. There was no correlation between the plasma encainide concentration obtained at the time of study and the magnitude of change in any electrophysiologic variable. It is concluded that (1) encainide depresses conduction in the A-V node, His-Purkinje system and accessory pathway, and increases refractoriness of the atrium, ventricle and accessory pathway, and (2) differences between these results and those of earlier studies using encainide in a single intravenous dose (which found no significant effects on A-V nodal conduction or atrial and ventricular refractoriness) may be explained in part by the effects of an active metabolite of encainide.
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