Abstract 16789: Activation Sequence within the Pulmonary Vein as the Driving Sources of Atrial Fibrillation: Three-dimensional Analysis Using a Non-contact Mapping System
Background: The mechanisms how the activation within the pulmonary vein (PV) drives the atrial fibrillation (AF) has not been elucidated.
Objectives: To define the AF maintenance mechanism by PV, we analyzed the activation sequence within the PV during AF.
Methods: Selective endocardial mapping of the left superior PV (LSPV) was performed during AF in 11 patients with paroxysmal AF using a three-dimensional non-contact mapping system (EnSite 3000). In addition, we analyzed how the circumferential radiofrequency energy applications around the LSPV alter the activation of the LSPV and terminate AF.
Results: Complex fractionated electrograms (CFE) were observed at the second half of the proximal LSPV at the roof (n=5), ridge (n=11) and carina (n=7). Mean CFE area was 9.1±3.4 cm2, which occupied the 19.8% of the LSPV area. Frequent episodes of pivoting activation associated with wave break and fusion was observed at this CFE area. The frequency of pivoting activation around the functional conduction block, wave break and fusion at the CFE region were significantly higher than those at the non-CFE region (32.5±12.2 vs. 4.6±5.8 times/sec; p<0.0001, 9.2±5.1 vs. 1.4±3.1 times/sec; p=0.0007, and 12.9±4.8 vs. 6.4±4.4 times/sec, p=0.0044). After isolation of ipsilateral right PV, subsequent circumferential radiofrequency energy applications around the left PV terminate the AF with a mean number of 13.5±7.8 applications, including LSPV roof (n=3.0±2.2) and LSPV ridge (n=5.6±1.9) lesions. AF was terminated before left PV isolation in all patients. The frequency of pivoting activation, wave break and fusion at all PV area just before the AF termination were significantly lower than those before ablation (8.1±11.7 vs. 37.0±14.7 times/sec; p<0.0001, 2.3±5.8 vs. 10.6±6.6 times/sec; p=0.005, 6.9±6.8 vs. 19.3±7.1 times/sec, p=0.0004), suggesting that linear lesion eliminate the random wave propagation over the CFE area.
Conclusions: AF was driven by the high frequent episodes of pivoting activation associated with wave break and wave fusion observed over the CFE area at the proximal PV. Linear lesions along the left PV including CFE area of the LSPV eliminate the meandering activation over the CFE area, resulting in the termination of AF.
Author Disclosures: H. Yamabe: Other Research Support; Modest; Medtronic Japan, Nihon Kohden, Boston scientific, St Jude Medical, Japan Lifeline, Fukuda Denshi, Neotec Japan, Shionogi. H. Kanazawa: Other Research Support; Modest; Medtronic Japan, Nihon Kohden, Boston scientific, St Jude Medical, Japan Lifeline, Fukuda Denshi, Neotec Japan, Shionogi. T. Hoshiyama: None. M. Ito: None. S. Kaneko: None. H. Ogawa: Other Research Support; Modest; Astellas Pharma Inc, Bristol-Myers Squibb Company, Chugai Pharmaceutical Co, Ltd, Dainippon Sumitomo Pharma Co., Ltd, MSD K.K, Mochida Pharmaceutical Co., Ltd, Ono Pharmaceutical Co., Ltd, Otsuka, Pfi. Other Research Support; Significant; Bayer, Daiichi Sankyo Co., Ltd, Novartis Pharma K.K, Sanofi K.K. Honoraria; Modest; AstraZeneca K.K, Boehringer Ingelheim Japan, Bristol-Myers Squibb Company, Mitsubishi Tanabe Pharma, Pfizer Japan Inc, Sanofi K.K, Teijin Pharma Co., Ltd. Honoraria; Significant; Bayer Yakuhin, Ltd, Daiichi Sankyo Co., Ltd, MSD K.K, Takeda Pharmaceutical Co., Ltd.
- © 2015 by American Heart Association, Inc.