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维拉帕米可抑制犬长期快速心房刺激模型中电重构的不均匀性。

Verapamil suppresses the inhomogeneity of electrical remodeling in a canine long-term rapid atrial stimulation model.

作者信息

Moriguchi Masahiko, Niwano Shinichi, Yoshizawa Naoto, Kojima Jisho, Inuo Kimiatsu, Izumi Tohru

机构信息

Department of Internal Medicine, Kitasato University School of Medicine, Sagamihara, Japan.

出版信息

Pacing Clin Electrophysiol. 2003 Nov;26(11):2072-82. doi: 10.1046/j.1460-9592.2003.00323.x.

DOI:10.1046/j.1460-9592.2003.00323.x
PMID:14622307
Abstract

Verapamil is known to suppress shortening of the atrial effective refractory period (AERP) during relatively short-term atrial pacing, although the effect of a long-term stimulation model is unclear. The effect of verapamil on electrical remodeling was evaluated in a canine rapid atrial stimulation model. The right atrial appendage (RAA) was continuously paced (400 beats/min) for 2 weeks. Four pairs of electrodes were sutured at four atrial sites; the RAA, right atrium close to the inferior vena cava, Bachmann's bundle, and LA. AERP, AERP dispersion (AERPd), conduction time, and inducibility of AF were evaluated during the pacing phase and the recovery phase. The same protocol was performed under the administration of verapamil. In five control dogs, the AERP shortening was inhomogeneous and the shortening of the AERP was most prominent in the LA. AERPd increased during the rapid pacing phase by 5 +/- 2 ms, but recovered quickly in the recovery phase. The max AERPd was 46 +/- 4 ms in the control group and was larger than that in the verapamil group (31 +/- 3 ms, P = 0.001). At the LA site, the shortening of the AERP was decreased by verapamil administration (-19 +/- 3 vs -5 +/- 2 ms, P = 0.04). However, the AF inducibility was not significantly different between the two groups. The effect of verapamil on electrical remodeling was inhomogeneous, depending on the anatomic portion. As a result, AERPd widening during the rapid pacing phase was suppressed by verapamil, while the AF inducibility was unchanged.

摘要

已知维拉帕米可抑制相对短期心房起搏期间心房有效不应期(AERP)的缩短,尽管长期刺激模型的效果尚不清楚。在犬快速心房刺激模型中评估了维拉帕米对电重构的影响。右心耳(RAA)持续起搏(400次/分钟)2周。在四个心房部位缝合四对电极;RAA、靠近下腔静脉的右心房、巴赫曼束和左心房(LA)。在起搏期和恢复期评估AERP、AERP离散度(AERPd)、传导时间和房颤诱导率。在给予维拉帕米的情况下执行相同方案。在五只对照犬中,AERP缩短不均匀,且在LA中AERP缩短最为明显。快速起搏期AERPd增加5±2毫秒,但在恢复期迅速恢复。对照组的最大AERPd为46±4毫秒,大于维拉帕米组(31±3毫秒,P = 0.001)。在LA部位,给予维拉帕米可减少AERP的缩短(-19±3对-5±2毫秒,P = 0.04)。然而,两组之间的房颤诱导率无显著差异。维拉帕米对电重构的影响不均匀,取决于解剖部位。结果,维拉帕米抑制了快速起搏期AERPd的增宽,而房颤诱导率未改变。

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