Ohkubo Kimie, Watanabe Ichiro, Takagi Yasuhiro, Okumura Yasuo, Ashino Sonoko, Kofune Masayoshi, Kofune Tatsuya, Shindo Atsushi, Sugimura Hidezou, Nakai Toshiko, Kunimoto Satoshi, Kasamaki Yuji, Saito Satoshi, Hirayama Atsushi
Division of Cardiology, Department of Medicine, Nihon University School of Medicine, Tokyo, Japan.
Circ J. 2007 Aug;71(8):1258-62. doi: 10.1253/circj.71.1258.
The pathogenesis of Brugada syndrome (BS) is reported to be phase 2 reentry resulting from shortening of the action potential duration at the epicardial site of the right ventricular outflow tract (RVOT). However, several reports have shown a high incidence of ventricular late potentials (LPs) and a high rate of induction of ventricular fibrillation (VF) by programmed ventricular stimulation (PVS) among patients with BS. The aim of this study was to investigate the role of slow conduction for the initiation of VF by PVS in these patients.
Endocardial mapping of the RVOT was conducted in 17 patients in whom VF was induced by PVS from the RV apex or RVOT; 11 patients had a positive LP. In 10 patients, RV mapping showed that low-amplitude fragmented and delayed potentials (DPs) were recorded at the RVOT below the pulmonary valve (PV) or between the PV and His bundle electrogram recording site. Electrograms recorded after PVS showed a high incidence of fractionated and disorganized DPs that lead to VF.
Slow conduction at the RVOT may contribute to the induction of VF by PVS. However, the role of slow conduction in spontaneous VF remains controversial.
据报道，Brugada综合征（BS）的发病机制是右心室流出道（RVOT）心外膜部位动作电位时程缩短导致的2期折返。然而，多项报告显示，BS患者中心室晚电位（LPs）的发生率较高，且程控心室刺激（PVS）诱发心室颤动（VF）的比例也较高。本研究的目的是探讨缓慢传导在这些患者中PVS诱发VF起始过程中的作用。
对17例由右心室心尖部或RVOT的PVS诱发VF的患者进行了RVOT的心内膜标测；11例患者LPs阳性。在10例患者中，RV标测显示在肺动脉瓣（PV）下方或PV与希氏束电图记录部位之间的RVOT记录到低振幅碎裂和延迟电位（DPs）。PVS后记录的电图显示，导致VF的碎裂和紊乱DPs发生率较高。
RVOT的缓慢传导可能有助于PVS诱发VF。然而，缓慢传导在自发性VF中的作用仍存在争议。
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