INTRODUCTION: Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. METHODS AND RESULTS: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 +/- 24 msec) by 89% to 309 +/- 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In five episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (+/- 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and subsequent termination. CONCLUSION: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.
INTRODUCTION:Flecainide is effective in terminating stable atrial flutter in the conscious dog with a Y-shaped right atrial lesion. In this model, flutter is due to circus movement of the impulse around a fixed anatomical barrier. METHODS AND RESULTS: To investigate the mechanism of flecainide-induced termination of this type of reentry, we determined the pattern of endocardial activation of the right and left atria before and during administration of flecainide by recording simultaneously from 192 electrode pairs in the isolated blood perfused heart. At least five consecutive flutter beats were analyzed before and during flecainide for each of eight termination episodes in five hearts. In all, flecainide increased flutter cycle length (164 +/- 24 msec) by 89% to 309 +/- 77 msec (P < 0.05) before termination. Atrial refractory period and conduction time during paced beats were also increased by flecainide. In five episodes, termination was due to conduction block of the impulse at critical sites within the reentrant circuit (mode 1). Cycle length oscillations (+/- 30 msec) at sites proximal to site of block preceded termination in three of these episodes. In three other episodes, interruption of the original circuit occurred when there was failure of a lateral boundary, giving rise to an impulse that reset the original circuit (mode 2). In these episodes, long-short cycle length oscillations led to return reexcitation by the impulse within the primary path and subsequent termination. CONCLUSION: In summary, similar to our previous findings with the Class III agent, d-sotalol, two different modes of termination of atrial reentry were observed with flecainide.