Transition mechanisms from atrial flutter to atrial fibrillation during anti-tachycardia pacing therapy.

Abstract

Atrial anti-tachycardia pacing (aATP) has been shown to be effective for the termination of atrial tachyarrhythmias, but its success rate is still not high enough. The main objective of this study was to investigate the mechanisms of atrial flutter (AFL) termination by aATP and the transition from AFL to atrial fibrillation (AF) during aATP. We developed a multi-scale model of the human atrium based on magnetic resonance images and examined the atrial electrophysiology of AFL during aATP with a ramp protocol. In successful cases of aATP, paced excitation entered the excitable gap and collided with the leading edge of the reentrant wave front. Furthermore, the excitation propagating in the opposite direction collided with the trailing edge of the reentrant wave to terminate AFL. The second collision was made possible by the distribution of the wave propagation velocity in the atria. The detailed analysis revealed that the slowing of propagation velocity occurred at the exit of the sub-Eustachian isthmus, probably due to source-sink mismatch. During the transition from AFL to AF, the excitation collided with the refractory zone of the preceding wave and broke into multiple wave fronts to induce AF. A similar observation was made for the transition from AF to sinus rhythm. In both cases, the complex anatomy of the atria played an essential role. The complex anatomy of atria plays an essential role in the maintenance of stable AFL and its termination by aATP, which were revealed by the realistic three-dimensional simulation model.