Ohkubo Kimie, Watanabe Ichiro, Okumura Yasuo, Takagi Yasuhiro, Ashino Sonoko, Kofune Masayoshi, Sugimura Hidezou, Nakai Toshiko, Kasamaki Yuji, Hirayama Atsushi, Morimoto Shin-Ichiro
Division of Cardiology, Department of Medicine, Nihon University School of Medicine.
Int Heart J. 2010 Jan;51(1):17-23. doi: 10.1536/ihj.51.17.
The reported pathogenesis of Brugada syndrome is phase 2 reentry resulting from shortening of the epicardial action potential duration at the right ventricular outflow tract (RVOT). However, several studies have revealed a high incidence of ventricular late potentials and high rate of ventricular fibrillation (VF) induced by programmed ventricular stimulation (PVS). The aim of the present study was to evaluate the role of slow conduction at the RVOT for the initiation of VF by PVS and any underlying pathological conditions in Brugada syndrome. Endocardial mapping of the RVOT and endomyocardial biopsy of the right ventricle were performed in 25 patients with Brugada syndrome with inducible VF. Late potentials were positive in 11 of the 25 (44%) patients. Low-amplitude fragmented and delayed electrograms were recorded at the RVOT in 13 of 18 (72.2%) patients. Histologic examination of the biopsy samples revealed fatty tissue infiltration, interstitial fibrosis, lymphocyte infiltration, and/or myocyte disorganization in 13 patients. Slow conduction at the RVOT may contribute to the induction of VF by PVS in Brugada syndrome. Various pathomorphologic changes may contribute to slow conduction at the RVOT.
据报道，Brugada综合征的发病机制是右心室流出道（RVOT）心外膜动作电位时程缩短导致的2期折返。然而，多项研究显示心室晚电位的发生率很高，且程控心室刺激（PVS）诱发心室颤动（VF）的比例也很高。本研究的目的是评估RVOT处缓慢传导在PVS诱发VF中的作用以及Brugada综合征的任何潜在病理状况。对25例可诱发性VF的Brugada综合征患者进行了RVOT的心内膜标测和右心室心内膜活检。25例患者中有11例（44%）的晚电位呈阳性。18例患者中有13例（72.2%）在RVOT记录到低振幅碎裂和延迟的电图。活检样本的组织学检查显示，13例患者存在脂肪组织浸润、间质纤维化、淋巴细胞浸润和/或心肌细胞排列紊乱。RVOT处的缓慢传导可能促使PVS诱发Brugada综合征患者的VF。各种病理形态学改变可能导致RVOT处的缓慢传导。
