Mechanism of Atrial Fibrillation Induced in the Left Atrial Volume-load Model

Research Project

Project/Area Number	13671411
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Single-year Grants
Section	一般
Research Field	Thoracic surgery
Research Institution	Nippon Medical School
Principal Investigator	NITTA Takashi Nippon Medical School, School of Medicine, Associate Professor, 医学部, 助教授 (40256954)
Co-Investigator(Kenkyū-buntansha)	MIYAGI Yasuo Nippon Medical School, School of Medicine, Fellow, 医学部, 助手 (00350116) KANNO Shigeto Nippon Medical School, School of Medicine, Fellow, 医学部, 助手 (20291718) 田中茂夫日本医科大学, 医学部, 教授 (70089720)
Project Period (FY)	2001 – 2003
Project Status	Completed (Fiscal Year 2003)
Budget Amount *help	¥3,500,000 (Direct Cost: ¥3,500,000) Fiscal Year 2003: ¥900,000 (Direct Cost: ¥900,000) Fiscal Year 2002: ¥2,100,000 (Direct Cost: ¥2,100,000) Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Keywords	atrial fibrillation / left atrium / volume load / pulmonary vein / 電気生理 / 高頻度刺激
Research Abstract	A new experimental model for atrial fibrillation was established and serial changes in the left atrial volume and atrial electrophysiologies were examined in 10 mongrel canines. The canines underwent a left subclavian artery to pulmonary artery shunt surgery through a left thoracotomy. Left atrial rapid pacing at a cycle length of 100 ma was started 1 week after the shunt surgery. All the animals exhibited progressive dilatation of the left atrium and developed severe heart failure. Three of 10 died in the early postoperative days and 1 developed pacing failure. Remaining 6 animals were subjected to the analysis. A brief period of repetitive activations were observed after a temporal suspension of the rapid pacing one week after the pacing. The duration of repetitive activation prolonged over time and all the animals developed persistent atrial fibrillation (>10 minutes) 4 weeks after the pacing. Atrial fibrillation intervals recorded at both atrial appendages were progressively shortened and the interval in the left atrial appendage was always shorter than at the right appendage. Epicardial mapping of the persistent atrial fibrillation revealed concurrent repetitive activations arising from the right and left superior pulmonary veins that conducted toward the right atrium with progressive conduction delay. A volume load of the LA may provoke repetitive activations in the pulmonary veins and electrical remodeling of the atrial myocardium, and further facilitate the perpetuation of atrial fibrillation. This clinically relevant model of persistent AF associated with a Volume-loaded LA would be useful in examining the electrophysiology of AF and the effects of non-pharmacological therapies.