Influence of propafenone on resetting and termination of canine atrial flutter

Previous studies on atrial flutter (AF) presumed that resetting was due to the prematurity effect (PE) in which the stimulated antegrade wavefront tra vels in the tail of the AF preexisting wavefront. We studied the collision effect (CE) between the AF and the stimulated retrograde wavefronts, its co ntribution to resetting, and its relationship to AF termination and how the y are affected by the Class IC agent propafenone (PPF). A canine model of A F 12 as created using a Y-shaped lesion in the right atrium in 14 dogs (33 +/- 3 kg). Five atrial bipolar electrodes were positioned around the tricus pid valve. In a subsequent set of 11 dogs, we used 16 bipolar electrodes fo r recording. AF was induced by burst pacing. Single and multiple stimuli we re applied to measure conduction time and reset-response curves (RRCs). Thi s was repeated after the administration of PPF (1 mg/kg loading dose for 10 minutes, followed by 1.8 mg/kg/per hour infusion). Three distinct mechanis ms were found to contribute to the RRC: the PE, the CE, and heterogeneity P PF stabilized the RRC, increased significantly the cycle length (CL), the d uration of the effective refractory period, as well as the duration of the excitable gap. However, PPF did not alter the duration of free fully excita ble portion, We studied 36 annihilations without and 48 with PPF. Transient fibrillation was found in 75% of the episodes without, compared to 22 % wi th PPF. Other types of termination such as conduction block, CL oscillation s, and reversal of activation were found for 25% of the episodes without an d 78% with PPF. In many cases, conduction block and CL oscillations were as sociated with a failure of propagation of the stimulated antegrade wavefron t in the region of collision. Termination by reversal of activation suggest s that propagation was two dimensional and could not be represented by a on e dimensional movement. The average coupling interval (in percent of CL), t hat induced fibrillation rr as not significantly different from that at whi ch conduction block occurred. This suggests that transient fibrillation is associated with a weak CE rather than with rapid pacing. The CE is amplifie d by multiple stimuli and PPF. The incidence of transient fibrillation in A F annihilation diminishes with PPF as the CE becomes more important. This s uggests that the evaluation of PE and CE in AF may be an indication of the risk of atrial fibrillation.