Aiba Takeshi, Shimizu Wataru, Hidaka Ichiro, Uemura Kazunori, Noda Takashi, Zheng Can, Kamiya Atsunori, Inagaki Masashi, Sugimachi Masaru, Sunagawa Kenji
Department of Cardiovascular Dynamics, Research Institute, National Cardiovascular Center, Suita, Japan.
J Am Coll Cardiol. 2006 May 16;47(10):2074-85. doi: 10.1016/j.jacc.2005.12.064. Epub 2006 Apr 24.
We examined how repolarization and depolarization abnormalities contribute to the development of extrasystoles and subsequent ventricular fibrillation (VF) in a model of the Brugada syndrome.
Repolarization and depolarization abnormalities have been considered to be mechanisms of the coved-type ST-segment elevation (Brugada-electrocardiogram [ECG]) and development of VF in the Brugada syndrome.
We used high-resolution (256 x 256) optical mapping techniques to study arterially perfused canine right ventricular wedges (n = 20) in baseline and in the Brugada-ECG produced by administration of terfenadine (5 micromol/l), pinacidil (2 micromol/l), and pilsicainide (5 micromol/l). We recorded spontaneous episodes of phase 2 re-entrant (P2R)-extrasystoles and subsequent self-terminating polymorphic ventricular tachycardia (PVT) or VF under the Brugada-ECG condition and analyzed the epicardial conduction velocity and action potential duration (APD) restitutions in each condition.
Forty-one episodes of spontaneous P2R-extrasystoles in the Brugada-ECG were successfully mapped in 9 of 10 preparations, and 33 of them were originated from the maximum gradient of repolarization (GR(max): 176 +/- 54 ms/mm) area in the epicardium, leading to PVT (n = 12) or VF (n = 5). The epicardial GR(max) was not different between PVT and VF. Wave-break during the first P2R-extrasystole produced multiple wavelets in all VF cases, whereas no wave-break or wave-break followed by wave collision and termination occurred in PVT cases. Moreover, conduction velocity restitution was shifted lower and APD restitution was more variable in VF cases than in PVT cases.
Steep repolarization gradient in the epicardium but not endocardium develops P2R-extrasystoles in the Brugada-ECG condition, which might degenerate into VF by further depolarization and repolarization abnormalities.
我们研究了复极化和去极化异常如何在Brugada综合征模型中导致期前收缩及随后的心室颤动（VF）的发生。
复极化和去极化异常被认为是Brugada综合征中穹窿型ST段抬高（Brugada心电图[ECG]）及VF发生的机制。
我们使用高分辨率（256×256）光学标测技术，研究在基线状态以及通过给予特非那定（5微摩尔/升）、吡那地尔（2微摩尔/升）和吡西卡尼（5微摩尔/升）产生Brugada-ECG时，动脉灌注的犬右心室楔形组织（n = 20）。我们记录了在Brugada-ECG条件下2相折返（P2R）-期前收缩的自发发作以及随后的自行终止的多形性室性心动过速（PVT）或VF，并分析了每种情况下的心外膜传导速度和动作电位时程（APD）恢复情况。
在10个标本中的9个成功标测到了Brugada-ECG中41次自发的P2R-期前收缩发作，其中33次起源于心外膜复极化最大梯度（GR(max)：176±54毫秒/毫米）区域，导致PVT（n = 12）或VF（n = 5）。PVT和VF之间的心外膜GR(max)无差异。在所有VF病例中，首次P2R-期前收缩期间的波裂产生了多个小波，而在PVT病例中未发生波裂或波裂后接着波碰撞和终止的情况。此外，与PVT病例相比，VF病例中的传导速度恢复曲线下移，APD恢复更具变异性。
在心外膜而非心内膜存在陡峭的复极化梯度会在Brugada-ECG条件下产生P2R-期前收缩，其可能通过进一步的去极化和复极化异常恶化为VF。
