Maintenance mechanism of paroxysmal atrial fibrillation from the activation occurring within the pulmonary vein: analysis using non-contact mapping.

It is unclear how pulmonary veins (PVs) maintain paroxysmal atrial fibrillation (AF). To clarify the PV's arrhythmogenic role, we examined PV activation sequences during paroxysmal AF. Left superior PV (LSPV) endocardial non-contact mapping was performed after a right PV isolation in 13 paroxysmal AF patients. Activation sequences within the LSPV before and during left-sided PVs ablation were analyzed, and those in complex fractionated atrial electrogram (CFAE) areas were compared with those in non-CFAE areas. CFAEs were observed in the LSPV's proximal half (area; 8.8 ± 3.2cm2) occupying 19.9 ± 6.0% of LSPV. The number of pivoting activations, wave breaks, and fusions over CFAE areas were significantly higher than those over non-CFE areas (25.5 ± 9.3 vs. 4.5 ± 4.8 times/s, p < 0.0001; 9.1 ± 5.3 vs. 1.4 ± 1.8 times/s, p < 0.0001; 13.0 ± 4.6 vs. 5.4 ± 4.4 times/s, p < 0.0001). The conduction velocities in CFAE areas were significantly slower than in non-CFAE areas (0.6 ± 0.2 vs. 1.7 ± 0.8 m/s, p < 0.001). After delivery of ablation lesions around the left-sided PVs (13.2 ± 7.4 applications), the PV activation became organized with a loss of CFAE areas, and the frequency of the LSPV's pivoting activation, wave break, and fusion significantly decreased compared to that pre-ablation (7.3 ± 10.9 vs. 30.0 ± 11.6 times/s, p < 0.001; 2.1 ± 5.3 vs. 10.5 ± 6.2 times/s, p < 0.002; 6.0 ± 6.6 vs. 18.4 ± 8.2 times/s, p < 0.001). Subsequently, AF terminated before the left-sided PV isolation in all patients. In conclusion, high-frequency random reentry associated with pivoting activation, wave break, and fusion within the LSPV, observed mostly over CFAE areas, maintained AF. Linear ablation lesions around the PV suppressed random reentry, resulting in the loss of CFAEs and AF termination.