Background
Complex fractionated electrograms (CFAE) are targets of atrial fibrillation (AF) ablation. Serial high density maps were evaluated to understand the impact of activation direction and rate on electrogram (EGM) fractionation.
Methods and Results
18 patients (9 persistent) underwent high density, 3D, left atrial mapping (>400 points/map) during AF, Sinus (SR) and CS-paced (CSp) rhythms. In SR and CSp, fractionation was defined as EGM with ≥4 deflections, while in AF CFEmean <80ms was considered as continuous CFAE. The anatomic distribution of CFAE sites was assessed, quantified and correlated between rhythms. Mechanisms underlying fractionation were investigated by analysis of voltage, activation and propagation maps. A minority of continuous CFAE sites displayed EGM fractionation in SR (15+/−4%) and CSp (12+/(12+/−8%). EGM fractionation did not match between SR and CSp at 70+/−10% sites. Activation maps in SR and CSp showed that wave collision (71%) and regional slow conduction (24%) caused EGM fractionation. EGM voltage during AF (0.59+/−0.58mV) was lower than during SR and CSp (>1.0mV) at all sites. During AF, the EGM voltage was higher at continuous CFAE sites than at non-CFAE sites (0.53mV (Q1, Q3: 0.33–0.83) vs. 0.30 mV (Q1, Q3: 0.18–0.515), p<0.00001). Global LA voltage in AF was lower in persistent vs. paroxysmal AF patients (0.6+/−0.59mV vs. 1.12+/−1.32mV, p<0.01).
Conclusions
The distribution of fractionated EGMs is highly variable, depending on direction and rate of activation (SR vs. CSp vs. AF). Fractionation in sinus and CSp rhythms mostly resulted from wave collision. All sites with continuous fractionation in AF displayed normal voltage in SR suggesting absence of structural scar. Thus, many fractionated EGMs are functional in nature and their sites dynamic.