Mechanisms of the preventive effect of pilsicainide on atrial fibrillation originating from the pulmonary vein.

Mechanisms of the preventive effect of pilsicainide on atrial fibrillation originating from the pulmonary vein.
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DOI:
10.1253/circj.71.1805
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发表时间:
2007-12
期刊:
Circulation journal : official journal of the Japanese Circulation Society
影响因子:
--
通讯作者:
M. Hirose;Yosuke Ohkubo;M. Takano;M. Hamazaki;T. Sekido;M. Yamada
M. Hirose;Yosuke Ohkubo;M. Takano;M. Hamazaki;T. Sekido;M. Yamada
中科院分区:
其他
文献类型:
--
作者:
M. Hirose;Yosuke Ohkubo;M. Takano;M. Hamazaki;T. Sekido;M. Yamada

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背景技术已经表明,匹西卡尼通过药理肺静脉(PV)隔离来终止心房颤动(AF)。然而,是否可以通过相同的机制阻止PV引起的房颤诱发仍不确定。方法和结果 在对 6 只麻醉犬的双侧颈迷走神经进行电刺激时以及在 8 只孤立的心房中输注乙酰胆碱 (ACh) 时,从左上 PV (LSPV) 和右心房游离壁 (RAF) 进行快速起搏以诱导 AF。在使用匹西卡尼之前,无论起搏部位如何,快速起搏都会在所有狗中诱发房颤。匹西卡尼 (1 mg/kg) 通过 LSPV 和左心房游离壁 (LAF) 之间的冲动传导阻滞,在 LSPV 快速起搏期间预防 AF。然而,当从 RAF 进行起搏​​时,相同剂量的匹西卡尼并不能预防 AF。在所有测试的隔离制剂中,匹西卡尼部分恢复了因输注乙酰胆碱而缩短的动作电位持续时间,并通过 LSPV-左心房交界处的冲动传导阻滞来预防 AF。结论 结果表明:(1) LSPV-LA 交界处的脉冲传导阻滞是 pilsicainide 诱导预防源自 LSPV 的迷走神经诱发 AF 的根本机制;(2) pilsicainide 在预防源自 LSPV 的 AF 方面比预防 RA 更有效。
BACKGROUND It has been shown that pilsicainide terminates atrial fibrillation (AF) by pharmacologic pulmonary vein (PV) isolation. However, whether it can prevent AF induction originating from the PV by the same mechanism is still uncertain. METHODS AND RESULTS Rapid pacing from the left superior PV (LSPV) and the right atrial free wall (RAF) was performed to induce AF during electrical stimulation of both cervical vagal nerves in 6 anesthetized dogs and during the infusion of acetylcholine (ACh) in 8 isolated atria. Rapid pacing induced AF in all dogs, regardless of the pacing site, before pilsicainide. Pilsicainide (1 mg/kg) prevented AF during rapid pacing from the LSPV, with an impulse conduction block between the LSPV and the left atrial free wall (LAF). However, the same dose of pilsicainide did not prevent AF when pacing was performed from the RAF. Pilsicainide partially restored the action potential duration shortened by ACh infusion and prevented AF with an impulse conduction block at the LSPV-left atrial junction in all isolated preparations tested. CONCLUSION The results suggest that (1) impulse conduction block at the LSPV-LA junction is the underlying mechanism of pilsicainide-induced prevention of vagally-induced AF originating from the LSPV and (2) pilsicainide is more effective at preventing AF originating from the LSPV than that from the RA.