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 (RP(AF)), conduction velocity (CV(AF)), pathlength (PL(AF)), wavelength (WL(AF)), temporal (AFCL-RP(AF)), and spatial (PL(AF)-WL(AF)) excitable gap were studied. The RP(AF) was measured by determining the earliest moment at which single stimuli could capture the fibrillating atria. CV(AF) was measured during regional entrainment of AF. Contrary to our expectation, cardioversion of AF could not be attributed to prolongation of WL(AF). Hydroquinidine and d-sotalol did not affect WL(AF) significantly, whereas cibenzoline and flecainide even shortened WL(AF) by 18% and 36%, respectively. PL(AF) was increased by hydroquinidine and d-sotalol by 30%, whereas cibenzoline and flecainide did not prolong PL(AF). 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 WL(AF). An alternative explanation for the antifibrillatory effect of class I and III drugs may be a widening of the temporal excitable gap.
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 (RP(AF)), conduction velocity (CV(AF)), pathlength (PL(AF)), wavelength (WL(AF)), temporal (AFCL-RP(AF)), and spatial (PL(AF)-WL(AF)) excitable gap were studied. The RP(AF) was measured by determining the earliest moment at which single stimuli could capture the fibrillating atria. CV(AF) was measured during regional entrainment of AF. Contrary to our expectation, cardioversion of AF could not be attributed to prolongation of WL(AF). Hydroquinidine and d-sotalol did not affect WL(AF) significantly, whereas cibenzoline and flecainide even shortened WL(AF) by 18% and 36%, respectively. PL(AF) was increased by hydroquinidine and d-sotalol by 30%, whereas cibenzoline and flecainide did not prolong PL(AF). 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 WL(AF). An alternative explanation for the antifibrillatory effect of class I and III drugs may be a widening of the temporal excitable gap.