Is Widening of the Excitable Gap Antifibrillatory?
Although cibenzoline, hydroquinidine, flecainide, and d-sotalol all were effective in cardioverting chronic AF, they exerted different effects on RPAF, CVAF, PLAF, and WLAF. The only action these 4 drugs had in common was a widening of the temporal excitable gap during AF. Although of course this does not prove anything, it raises the question of whether the antifibrillatory drug action is caused by a widening of the excitable gap. According to Moe’s multiple-wavelet hypothesis, the stability of AF is determined by the average number of wavelets. 1 Mapping studies have indicated that during AF, the number of wavelets varies considerably as a result of variation in rate of wave formation and extinction. 2–4 Because the life span of fibrillation waves is rather short, the rate of wavelet formation must be high. The exact mechanism of wavelet generation during AF is still poorly understood. Foci of abnormal automaticity, 17,18 multiple offsprings of a mother wave or a rotor, 19,20 and bif
