Background: The precise mechanisms of random wave propagation perpetuated after pulmonary vein isolation (PVI) in atrial fibrillation (AF) has not been well clarified. Objectives: The purpose of this study was to define the mechanism of random wave propagation perpetuated after PVI in AF. We further clarified the difference in this perpetuating mechanism between paroxysmal and persistent AF. Methods: Endocardial mapping of the left atrium was performed before and after PVI in 7 paroxysmal and 7 persistent AF patients using a three-dimensional non-contact mapping system (EnSite 3000). We analyzed the difference in the left atrial activation sequence between paroxysmal and persistent AF, especially in relation to the complex fractionated electrograms (CFAE) region. Results: Random wave propagation after PVI was maintained by the combination of focal discharge, the activation around the isolated PV and mitral annulus, wave break and pivoting activation anchored around the functional conduction block region. The frequency of pivoting activation, wave break and wave fusion were significantly higher in the persistent AF than in the paroxysmal AF (8.4±10.4 vs. 2.0±3.5 times/sec; p<0.001, 1.9±3.2 vs. 0±0 times/sec; p<0.05, and 12.1±3.3 vs. 6.3±13.4 times/sec; p<0.005). However, the frequency of focal discharge derived from non-PV region in persistent AF was lower than in paroxysmal AF (0.3±0.6 vs. 3.2±8.8 times/sec; p<0.03). The area of CFAE was significantly reduced following PVI both in paroxysmal and persistent AF (18.0±16.9 to 2.2±4.9 cm 2 ; p<0.0001, 26.8±22.3 to 6.6±2.9 cm 2 ; p<0.0001). However, the area of CFAE in persistent AF was significantly larger than that in paroxysmal AF both before (p=0.003) and after PVI (p<0.002). Pivoting activation and wave break were observed on the residual CFAE region which was still observed after PVI. Conclusions: Activation sequence of the wave during ongoing AF perpetuated after PVI was more disorganized in persistent AF than in paroxysmal AF. Disorganized activation after PVI in persistent AF was caused by the pivoting activation and wave break associated with the residual CFAE region.
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