Rodríguez Blanca, Trayanova Natalia
Department of Biomedical Engineering, Tulane University, New Orleans, LA 70118, USA.
J Electrocardiol. 2003;36 Suppl:51-6. doi: 10.1016/j.jelectrocard.2003.09.066.
The goal of this modeling study is to investigate the mechanisms responsible for the upper and lower limits of vulnerability (ULV and LLV) to re-entry induced by electric shocks within the three-dimensional volume of the heart. We use a geometrically accurate rabbit ventricular model with realistic fiber architecture that also includes the blood in the cavities and a perfusing bath. The shocks are delivered over a range of strengths and coupling intervals via two large mesh electrodes located at the vertical boundaries of the perfusing bath. Our results demonstrate that shock-induced virtual electrode polarization (VEP) in the midmyocardium is weaker and more complex than VEP on the surfaces, where only 2 areas, one of positive and one of negative polarization, are induced. Transmural views of the ventricles show that, in all cases, tissue in the LV free wall and in the septum is deexcited by the shock providing an excitable path for wavefront propagation. Conversely, the RV free wall myocardium is depolarized after the end of the shock. The evolution of postshock electrical activity in the RV free wall plays a critical role in determining the outcome of the shock. In all cases, a wavefront starts in the apex at the site of largest transmembrane voltage gradient between oppositely polarized areas. For shocks of strength above the LLV, the postshock refractoriness of the RV free wall produces the unidirectional block necessary for reentry induction. If shock strength is below the ULV, the RV free wall recovers in time to provide the reentrant pathway. In contrast, for shocks of strength above the ULV, the postshock excitable gap in the LV free wall and in the septum is depolarized before the RV free wall recovers. Therefore, both ventricles are refractory and reentry is not induced
本建模研究的目的是探究在心脏三维容积内，电击诱发折返的易损性上限和下限（ULV和LLV）的相关机制。我们使用了一个具有逼真纤维结构的几何精确的兔心室模型，该模型还包括心腔内的血液和灌注浴。电击通过位于灌注浴垂直边界的两个大网格电极，在一系列强度和耦合间期下施加。我们的结果表明，心肌中层由电击诱发的虚拟电极极化（VEP）比表面的VEP更弱且更复杂，表面仅诱发两个区域，一个是正极化区域，一个是负极化区域。心室的透壁视图显示，在所有情况下，左心室游离壁和室间隔的组织因电击而除极，为波前传播提供了一条可兴奋路径。相反，右心室游离壁心肌在电击结束后发生去极化。右心室游离壁电击后电活动的演变在决定电击结果中起关键作用。在所有情况下，一个波前在相反极化区域之间跨膜电压梯度最大的部位的心尖处起始。对于强度高于LLV的电击，右心室游离壁电击后的不应期产生了诱发折返所需的单向阻滞。如果电击强度低于ULV，右心室游离壁及时恢复以提供折返途径。相反，对于强度高于ULV的电击，左心室游离壁和室间隔电击后的可兴奋间隙在右心室游离壁恢复之前就已去极化。因此，两个心室均处于不应期，未诱发折返。
