血管紧张素II 1型受体拮抗剂对心房颤动电重构和结构重构的影响。

Effects of angiotensin II type 1 receptor antagonist on electrical and structural remodeling in atrial fibrillation.

作者信息

Kumagai Koichiro, Nakashima Hideko, Urata Hidenori, Gondo Naoki, Arakawa Kikuo, Saku Keijiro

机构信息

Department of Cardiology, School of Medicine, Fukuoka University, Fukuoka, Japan.

出版信息

J Am Coll Cardiol. 2003 Jun 18;41(12):2197-204. doi: 10.1016/s0735-1097(03)00464-9.

DOI:10.1016/s0735-1097(03)00464-9

PMID:12821247

Abstract

UNLABELLED

The purpose of the present study was to evaluate the effect of angiotensin II type 1 receptor (AT1R) antagonist on chronic structural remodeling in atrial fibrillation (AF).

BACKGROUND

We previously reported that an AT1R antagonist, candesartan, prevents acute electrical remodeling in a rapid pacing model. However, the effect of candesartan on chronic structural remodeling in AF is unclear.

METHODS

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 beats/min for five weeks. Candesartan was administered orally (10 mg/kg/day) for one week before rapid pacing and was continued for five weeks. The AF duration, atrial effective refractory period (AERP) at four sites in the RA, and intra-atrial conduction time (CT) from the RA appendage to the other three sites were measured every week.

RESULTS

The mean AF duration in the control group after five weeks was significantly longer than that with candesartan (1,333 +/- 725 vs. 411 +/- 301 s, p < 0.01). The degree of AERP shortening after five weeks was not significantly different between the two groups. The CT from the RA appendage to the low RA after five weeks with candesartan was significantly shorter than that in the control (43 +/- 14 vs. 68 +/- 10 ms, p < 0.05). The candesartan group had a significantly lower percentage of interstitial fibrosis than the control group (7 +/- 2% vs. 16 +/- 1% at the RA appendage, p < 0.001).

CONCLUSIONS

Candesartan can prevent the promotion of AF by suppressing the development of structural remodeling.

摘要

未标记

本研究的目的是评估1型血管紧张素II受体（AT1R）拮抗剂对心房颤动（AF）慢性结构重塑的影响。

背景

我们之前报道过，AT1R拮抗剂坎地沙坦可在快速起搏模型中预防急性电重塑。然而，坎地沙坦对AF慢性结构重塑的影响尚不清楚。

方法

通过以400次/分钟的频率快速起搏右心房（RA）五周，在20只犬（对照组10只，坎地沙坦组10只）中诱导持续性AF。在快速起搏前一周口服坎地沙坦（10毫克/千克/天），并持续五周。每周测量AF持续时间、RA四个部位的心房有效不应期（AERP）以及从RA附件到其他三个部位的心房内传导时间（CT）。

结果

五周后对照组的平均AF持续时间显著长于坎地沙坦组（1333±725秒对411±301秒，p<0.01）。两组五周后AERP缩短程度无显著差异。坎地沙坦组五周后从RA附件到低位RA的CT显著短于对照组（43±14毫秒对68±10毫秒，p<0.05）。坎地沙坦组的间质纤维化百分比显著低于对照组（RA附件处为7±2%对16±1%，p<0.001）。