Abstract 9976: Human Atrial Fibrillation Initiates by Formation of a Dominant Spiral Wave at the Site Where Triggers Cause Dynamic Conduction Slowing
Introduction Triggers may initiate human atrial fibrillation (AF), but by unclear mechanisms. We hypothesized that triggers would dynamically slow atrial conduction velocity, to enable the formation of a single localized spiral wave or repetitive focal beat that may drive the atria into AF.
Methods We studied 13 patients at clinically-indicated AF ablation (5 persistent, age 63±11 years, LA size 43±6mm) in whom we placed 64-pole basket catheters (Boston Scientific, Natick, MA) in both atria. AF was initiated by accelerating pacing initially from 120 beats/min to AF onset. We constructed isochronal maps of both atria for beats leading to and including the first cycles of AF. We computed conduction time to each bi-atrial electrode at each rate, thus defining rate-dependence (restitution) of conduction throughout the atria.
Results AF initiated in the left atrium in 13/13 patients. Notably, atrial conduction slowed dynamically with rate at the site of AF onset in 8 patients, either gradually (Figure A) or abruptly. In all patients, spatial mapping showed that triggers initiated AF at a site of dynamic conduction slowing (76%±60%) by the formation of a single spiral wave (n=7; figure B) or repetitive focal beat (n=1). Notably, these regions were not the slowest to activate at baseline. Figure A shows dynamic conduction velocity slowing only at faster rates (Fig A, steep curve) at a site in the septal posterior LA, which enabled block (Figure B, site marked *) and formation of a spiral wave (Fig B, curved arrow) that initiates AF.
Conclusions Triggers initiate human AF by causing dynamic conduction slowing, enabling the formation of a single reentrant spiral wave (or repetitive focal beat) that drives the atria into AF. Of note, these sites did not exhibit conduction slowing at baseline, showing the central dynamic role of the trigger in AF initiation. Future studies should modulate conduction slowing from a trigger to prevent AF initiation.
- © 2012 by American Heart Association, Inc.