Ashihara Takashi, Constantino Jason, Trayanova Natalia A
Department of Cardiovascular Medicine, Shiga University of Medical Science, Otsu, Japan.
Circ Res. 2008 Mar 28;102(6):737-45. doi: 10.1161/CIRCRESAHA.107.168112. Epub 2008 Jan 24.
Comprehensive understanding of the ventricular response to shocks is the approach most likely to succeed in reducing defibrillation threshold. We propose a new theory of shock-induced arrhythmogenesis that unifies all known aspects of the response of the heart to monophasic (MS) and biphasic (BS) shocks. The central hypothesis is that submerged "tunnel" propagation of postshock activations through shock-induced intramural excitable areas underlies fibrillation induction and the existence of isoelectric window. We conducted simulations of fibrillation induction using a realistic bidomain model of rabbit ventricles. Following pacing, MS and BS of various strengths/timings were delivered. The results demonstrated that, during the isoelectric window, an activation originated deep within the ventricular wall, arising from virtual electrodes; it then propagated fully intramurally through an excitable tunnel induced by the shock, until it emerged onto the epicardium, becoming the earliest-propagated postshock activation. Differences in shock outcomes for MS and BS were found to stem from the narrower BS intramural postshock excitable area, often resulting in conduction block, and the difference in the mechanisms of origin of the postshock activations, namely intramural virtual electrode-induced phase singularity for MS and virtual electrode-induced propagated graded response for BS. This study provides a novel analysis of the 3D mechanisms underlying the origin of postshock activations in the process of fibrillation induction by MS and BS and the existence of isoelectric window. The tunnel propagation hypothesis could open a new avenue for interventions exploration to achieve significantly lower defibrillation threshold.
全面了解心室对电击的反应是最有可能成功降低除颤阈值的方法。我们提出了一种新的电击诱发心律失常的理论，该理论统一了心脏对单相（MS）和双相（BS）电击反应的所有已知方面。核心假设是，电击后激活通过电击诱发的壁内可兴奋区域的淹没“隧道”传播是颤动诱发和等电窗存在的基础。我们使用兔心室的真实双域模型进行了颤动诱发的模拟。起搏后，施加各种强度/时间的MS和BS。结果表明，在等电窗期间，一个激活起源于心室壁深处，由虚拟电极产生；然后它通过电击诱发的可兴奋隧道在壁内完全传播，直到出现在心外膜上，成为最早传播的电击后激活。发现MS和BS电击结果的差异源于BS壁内电击后可兴奋区域较窄，常导致传导阻滞，以及电击后激活起源机制的差异，即MS的壁内虚拟电极诱发的相位奇点和BS的虚拟电极诱发的传播分级反应。本研究对MS和BS诱发颤动过程中电击后激活起源的三维机制以及等电窗的存在进行了新颖的分析。隧道传播假说可能为探索干预措施以实现显著更低的除颤阈值开辟一条新途径。
