Effect of PPAR-gamma activation and AT-II receptor blockade on electrical and structural substrate of atrial fibrillation.

Research Project

Project/Area Number	24591039
Research Category	Grant-in-Aid for Scientific Research (C)
Allocation Type	Multi-year Fund
Section	一般
Research Field	Circulatory organs internal medicine
Research Institution	University of Toyama
Principal Investigator	NISHIDA Kunihiro 富山大学, 大学病院, 助教 (40591631)
Co-Investigator(Renkei-kenkyūsha)	INOUE Hiroshi 富山大学, 事務局, 理事・副学長 (60151619)
Project Period (FY)	2012-04-01 – 2015-03-31
Project Status	Completed (Fiscal Year 2014)
Budget Amount *help	¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000) Fiscal Year 2014: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000) Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000) Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Keywords	心房細動 / リモデリング / アンジオテンシン / ペルオキシソーム増殖因子活性化受容体γ / 心房リモデリング
Outline of Final Research Achievements	Irbesartan possesses angiotensin receptor blocking and peroxisome proliferator activated receptor gamma activating properties, and has demonstrated protective effect against atrial fibrillation (AF) in various situations. The effects of irbesartan were determined in a canine atrial tachypacing model. Beagles were subjected to atrial tachypacing for 4 weeks and either placebo (control dogs) or irbesartan (irbesartan dogs) was given through the study period. After 4 weeks of tachypacing, left ventricular diastolic dimension increased and left ventricular ejection fraction decreased for similar extent in both groups. AF duration increased in control dogs, but this change was suppressed in irbesartan dogs. AF inducibility also had a tendency to be suppressed in irbesartan dogs. Atrial effective refractory period was similarly shortened in both groups. Irbesartan suppressed AF development despite similar extent of left ventricular dysfunction in a canine atrial tachypacing model.