Widening of the excitable gap during pharmacological cardioversion of atrial fibrillation in the goat -: Effects of cibenzoline, hydroquinidine, flecainide, and d-sotalol

Background-Previous studies suggest that the antifibrillatory action of class I and III drugs is due to prolongation of the atrial wavelength. The aim of the present study was to directly evaluate the electrophysiological action of antifibrillatory drugs in a goat model of chronic atrial fibrillation (AF). Methods and Results-Six goats were instrumented with multiple atrial electrodes, and sustained AF was induced by electrical remodeling. During sustained AF, the effects of intravenous infusion of cibenzoline, hydroquinidine, flecainide, and d-sotalol on AF cycle length (AFCL), refractory period (RPAF), conduction velocity (CVAF), pathlength (PLAF), wavelength (WLAF), temporal (AFCL-RPAF), and spatial (PLAF-WLAF) excitable gap were studied. The RPAF was measured by determining the earliest moment at which single stimuli could capture the fibrillating atria. CVAF was measured during regional entrainment of AF. Contrary to our expectation, cardioversion of AF could not be attributed to prolongation of WLAF. Hydroquinidine and d-sotalol did not affect WLAF significantly, whereas cibenzoline and flecainide even shortened WLAF by 18% and 36%, respectively. PLAF was increased by hydroquinidine and d-sotalol by 30%, whereas cibenzoline and flecainide did not prolong PLAF. The only parameter that correlated consistently with cardioversion of AF was a widening of the temporal excitable gap (cibenzoline 176%, hydroquinidine 105%, flecainide 86%, d-sotalol 88%). Conclusions-Pharmacological cardioversion of AF cannot be explained by prolongation of WLAF. An alternative explanation for the antifibrillatory effect of class I and III drugs may be a widening of the temporal excitable gap.