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持续性心房颤动导致的人体房室结电重构

Electrical Remodeling of the Atrioventricular Node Caused by Persistent Atrial Fibrillation in Humans.

作者信息

Sairaku Akinori, Nakano Yukiko, Suenari Kazuyoshi, Tokuyama Takehito, Kawazoe Hiroshi, Matsumura Hiroya, Tomomori Shunsuke, Amioka Michitaka, Kihara Yasuki

机构信息

Department of Cardiovascular Medicine, Hiroshima University Graduate School of Biomedical and Health Sciences, Hiroshima, Japan.

出版信息

J Cardiovasc Electrophysiol. 2016 Aug;27(8):918-22. doi: 10.1111/jce.12996. Epub 2016 May 12.

Abstract

BACKGROUND

An animal experiment showed that long-term atrial pacing or persistent atrial fibrillation (AF) caused electrical remodeling of the atrioventricular (AV) node. We aimed to test the hypothesis that persistent AF decreases the AV conductivity in human hearts.

METHODS AND RESULTS

We retrospectively compared the cardiac electrophysiological properties between patients with paroxysmal AF who underwent catheter ablation (PXAF, N = 254) and those with persistent or longstanding persistent AF (PSAF, N = 213). The PSAF patients were more likely than PXAF patients to have longer atrial-His (AH) (96.3 ± 25.7 vs. 91.3 ± 20.4 milliseconds; P = 0.02) and His-ventricle (HV) (43.1 ± 9.4 vs. 41.2 ± 8.6 milliseconds; P = 0.02) intervals. The AV nodal effective refractory period (ERP) (299.1 ± 74.6 vs. 276.2 ± 58.9 milliseconds; P < 0.001) and Wenckebach cycle length (420.9 ± 80.3 vs. 386 ± 58.6 milliseconds; P < 0.001) were also more prolonged in the PSAF patients. We found a dual AV nodal physiology with a similar frequency in both groups. The AH interval, fast pathway ERP, and Wenckebach cycle length in the PSAF patients were more likely than in the PXAF patients to be prolonged among the patients without dual pathways, while those intergroup differences were never seen among the patients with dual pathways. In subgroup analyses including only PSAF patients, there was no difference in the AV conductivity between the patients with persistent AF and those with longstanding persistent AF.

CONCLUSIONS

Persistent AF may cause a mild decrease in the AV nodal function in human hearts. Electrical remodeling may be uncommon if dual AV nodal pathways are present, and its extent may not depend on the duration of persistent AF.

摘要

背景

一项动物实验表明,长期心房起搏或持续性心房颤动(AF)会导致房室(AV)结发生电重构。我们旨在验证持续性房颤会降低人体心脏房室传导性这一假设。

方法与结果

我们回顾性比较了接受导管消融的阵发性房颤患者(PXAF,N = 254)和持续性或长期持续性房颤患者(PSAF,N = 213)的心脏电生理特性。PSAF患者比PXAF患者更有可能出现更长的心房 - 希氏束(AH)间期(96.3±25.7对91.3±20.4毫秒;P = 0.02)和希氏束 - 心室(HV)间期(43.1±9.4对41.2±8.6毫秒;P = 0.02)。PSAF患者的房室结有效不应期(ERP)(299.1±74.6对276.2±58.9毫秒;P < 0.001)和文氏周期长度(420.9±80.3对386±58.6毫秒;P < 0.001)也延长得更多。我们在两组中发现了频率相似的双房室结生理现象。在无双房室结通路的患者中,PSAF患者的AH间期、快径ERP和文氏周期长度比PXAF患者更有可能延长,而在有双房室结通路的患者中未观察到组间差异。在仅包括PSAF患者的亚组分析中,持续性房颤患者和长期持续性房颤患者之间的房室传导性没有差异。

结论

持续性房颤可能会导致人体心脏房室结功能轻度下降。如果存在双房室结通路,电重构可能不常见,其程度可能不取决于持续性房颤的持续时间。

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