Project/Area Number |
11670725
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Fukuoka University |
Principal Investigator |
KUMAGAI Koichiro School of Medicien, Fukuoka University Lecturer, 医学部, 講師 (10248510)
|
Co-Investigator(Kenkyū-buntansha) |
URATA Hidenori School of Medicien, Fukuoka University Lectruer, 医学部, 講師 (30289524)
IDEISHI Munehito School of Medicine, Fukuoka University Professor, 医学部, 教授 (20131807)
|
Project Period (FY) |
1999 – 2001
|
Project Status |
Completed (Fiscal Year 2001)
|
Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
|
Keywords | atrial fibrillation / remodeling / renin-angiotensin system / angiotensin II receptor antagonist / candesartan / electrophysiology / refractory period / conduction / アンジオテンシン / 心房 / 細動 |
Research Abstract |
Conclusion : Candesartan can prevent the structural remodeling that promotes AF by decreasing the AERP dispersion and conduction delay caused by interstitial fibrosis Background : We previously reported that an angiotensin II type 1 receptor antagonist, candesartan, prevents acute electrical remodeling in a rapid pacing model. However, the effect of angiotensin II type 1 receptor blockade on chronic structural remodeling in atrial fibrillation (AF) is unclear. Methods and Results : Sustained AF was induced in 20 dogs (10 in a control group and 10 in a candesartan group) by rapid pacing of the right atrium (RA) at 400 bpm for 5 weeks. Candesartan was administered orally (10mg/kg/day) for 1week before rapid pacing, and was continued for 5 weeks. The AF duration, atrial P, effective refractory period (AERP) at 4 sites in the RA and intra-atrial conduction time (CT) from the RA appendage to the other 3 sites were measured every week. The mean AF duration in the control was significantly longer than that with candesartan (1333±725 versus 411±301 sec, p<0.05). The degree of AERP shortening after 5 weeks was not significantly different between the two groups, however, the dispersion of AERP after 5 weeks with candesartan was significantly less than that in the control (20±9 versus 6±3 msec, p<0.05). CT after 5 weeks with candesartan was significantly shorter than that in the control (68±10 versus 43±14 msec, p<0.05). The candesartan group had a significantly lower percentage of interstitial fibrosis than the control group (16±1 versus 7±2%, p<0.05).
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