Electrogram fractionation during sinus rhythm occurs in normal voltage atrial tissue in patients with atrial fibrillation.

Abstract

Electrogram (EGM) fractionation is often associated with diseased atrial tissue; however, mechanisms for fractionation occurring above an established threshold of 0.5mV have never been characterized. We sought to investigate during sinus rhythm (SR) the mechanisms underlying bipolar EGM fractionation with high-density mapping in patients with atrial fibrillation (AF). Forty-five patients undergoing AF ablation (73% paroxysmal, 27% persistent) were mapped at high density (18562±2551 points) during SR (Rhythmia). Only bipolar EGMs with voltages above 0.5mV were considered for analysis. When fractionation (>40ms and >4 deflections) was detected, we classified the mechanisms as slow conduction, wave-front collision, or a pivot point. The relationship between EGM duration and amplitude, and tissue anisotropy and slow conduction, was then studied using a computational model. Of the 45 left atria analyzed, 133 sites of EGM fragmentation were identified with voltages above 0.5mV. The most frequent mechanism (64%) was slow conduction (velocity 0.45m/s±0.2) with mean EGM voltage of 1.1±0.5mV and duration of 54.9±9.4ms. Wavefront collision was the second most frequent (19%), characterized by higher voltage (1.6±0.9mV) and shorter duration (51.3±11.3ms). Pivot points (9%) were associated with the highest degree of fractionation with 70.7±6.6ms and 1.8±1mV. In 10 sites (8%) fractionation was unexplained. The EGM duration was significantly different among the 3 mechanisms (p=.0351). In patients with a history of AF, EGM fractionation can occur at amplitudes>0.5mV when in SR in areas often considered not to be diseased tissue. The main mechanism of EGM fractionation is slow conduction, followed by wavefront collision and pivot sites.