Influence of propafenone on resetting and termination of canine atrial flutter.

Abstract

Previous studies on atrial flutter (AF) presumed that resetting was due to the prematurity effect (PE) in which the stimulated antegrade wavefront travels in the tail of the AF preexisting wavefront. We studied the collision effect (CE) between the AF and the stimulated retrograde wavefronts, its contribution to resetting, and its relationship to AF termination and how they are affected by the Class IC agent propafenone (PPF). A canine model of AF was created using a Y-shaped lesion in the right atrium in 14 dogs (33 +/- 3 kg). Five atrial bipolar electrodes were positioned around the tricuspid valve. In a subsequent set of 11 dogs, we used 16 bipolar electrodes for recording. AF was induced by burst pacing. Single and multiple stimuli were applied to measure conduction time and reset-response curves (RRCs). This 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 mechanisms were found to contribute to the RRC: the PE, the CE, and heterogeneity. PPF stabilized the RRC, increased significantly the cycle length (CL), the duration of the effective refractory period, as well as the duration of the excitable gap. However, PPF did not alter the duration of the fully excitable portion. We studied 36 annihilations without and 48 with PPF. Transient fibrillation was found in 75% of the episodes without, compared to 22% with PPF. Other types of termination such as conduction block, CL oscillations, and reversal of activation were found for 25% of the episodes without and 78% with PPF. In many cases, conduction block and CL oscillations were associated with a failure of propagation of the stimulated antegrade wavefront in the region of collision. Termination by reversal of activation suggests that propagation was two dimensional and could not be represented by a one dimensional movement. The average coupling interval (in percent of CL), that induced fibrillation was not significantly different from that at which conduction block occurred. This suggests that transient fibrillation is associated with a weak CE rather than with rapid pacing. The CE is amplified by multiple stimuli and PPF. The incidence of transient fibrillation in AF annihilation diminishes with PPF as the CE becomes more important. This suggests that the evaluation of PE and CE in AF may be an indication of the risk of atrial fibrillation.