Cardiac ventricular tachycardia (VT) is a life-threatening arrhythmia consisting of a well organized structure of reentrant electrical excitation pathways. Understanding the generation and maintenance of the reentrant mechanisms, which lead to the onset of VT induced by premature beats in presence of infarct scar, is one of the most important issues in current electrocardiology. We investigate, by means of numerical simulations, the role of infarct scar dimension, repolarization properties and anisotropic fiber structure of scar tissue border zone (BZ) in the genesis of VT. The simulations are based on the Bidomain model, a reaction-diffusion system of Partial Differential Equations, discretized by finite elements in space and implicit-explicit finite differences in time. The computational domain adopted is an idealized left ventricle affected by an infarct scar extending transmurally. We consider two different scenarios: i) the scar region extends along the entire transmural wall thickness, from endocardium to epicardium, with the exception of a BZ region shaped as a central sub-epicardial channel (CBZ); ii) the scar region extends transmurally along the ventricular wall, from endocardium to a sub-epicardial surface, and is surrounded by a BZ region (EBZ). In CBZ simulations, the results have shown that: i) the scar extent is a crucial element for the genesis of reentry; ii) the repolarization properties of the CBZ, in particular the reduction of IKs and IKr currents, play an important role in the genesis of reentrant VT. In EBZ simulations, since the possible reentrant pathway is not assigned a-priori, we investigate in depth where the entry and exit sites of the cycle of reentry are located and how the functional channel of reentry develops. The results have shown that: i) the interplay between the epicardial anisotropic fiber structure and the EBZ shape strongly affects the propensity that an endocardial premature stimulus generates a cycle of reentry; ii) reentrant pathways always develop along the epicardial fiber direction; iii) very thin EBZs rather than thick EBZs facilitate the onset of cycles of reentry; iv) the sustainability of cycles of reentry depends on the endocardial stimulation site and on the interplay between the epicardial breakthrough site, local fiber direction and BZ rim.

中文翻译：

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梗塞疤痕尺寸，边界区复极化特性和各向异性在心脏折返的起源和维持中的作用。

心脏室性心动过速（VT）是威胁生命的心律失常，由折返电激发途径的组织良好的结构组成。了解折返机制的产生和维持，这导致梗塞疤痕存在时过早搏动诱发室速发作，是当前心电学中最重要的问题之一。我们通过数值模拟的方法调查室速的起源中，梗塞疤痕尺寸，复极化特性和疤痕组织边界区（BZ）的各向异性纤维结构的作用。这些模拟基于双域模型，该模型是偏微分方程的反应扩散系统，由空间中的有限元素和时间上的隐式-显式有限差分离散。所采用的计算域是理想的左心室，其受经壁延伸的梗塞疤痕影响。我们考虑两种不同的情况：i）瘢痕区域从心内膜到心外膜沿整个跨壁壁厚度延伸，但BZ区域的形状为中央心外膜下通道（CBZ）除外；ii）疤痕区域从心内膜到心外膜下表面沿心室壁透壁延伸，并被BZ区域（EBZ）围绕。在CBZ模拟中，结果表明：i）疤痕程度是折返发生的关键因素；ii）CBZ的复极化特性，特别是IKs和IKr电流的减少，在折返性VT的发生中起重要作用。在EBZ模拟中，由于未将可能的折返途径分配为先验，我们深入研究再入循环的入口和出口位置，以及再入功能通道的发展方式。结果表明：i）心外膜各向异性纤维结构和EBZ形状之间的相互作用强烈影响心内膜过早刺激产生折返循环的倾向；ii）折返途径始终沿心外膜纤维方向发展；iii）较薄的EBZ而不是较厚的EBZ促进了折返循环的开始；iv）再入循环的可持续性取决于心内膜刺激部位以及心外膜突破部位，局部纤维方向和BZ边缘之间的相互作用。结果表明：i）心外膜各向异性纤维结构和EBZ形状之间的相互作用强烈影响心内膜过早刺激产生折返循环的倾向；ii）折返途径始终沿心外膜纤维方向发展；iii）较薄的EBZ而不是较厚的EBZ促进了折返循环的开始；iv）再入循环的可持续性取决于心内膜刺激部位以及心外膜突破部位，局部纤维方向和BZ边缘之间的相互作用。结果表明：i）心外膜各向异性纤维结构和EBZ形状之间的相互作用强烈影响心内膜过早刺激产生折返循环的倾向；ii）折返途径始终沿心外膜纤维方向发展；iii）较薄的EBZ而不是较厚的EBZ促进了折返循环的开始；iv）再入循环的可持续性取决于心内膜刺激部位以及心外膜突破部位，局部纤维方向和BZ边缘之间的相互作用。iii）较薄的EBZ而不是较厚的EBZ促进了折返循环的开始；iv）再入循环的可持续性取决于心内膜刺激部位以及心外膜突破部位，局部纤维方向和BZ边缘之间的相互作用。iii）较薄的EBZ而不是较厚的EBZ促进了折返循环的开始；iv）再入循环的可持续性取决于心内膜刺激部位以及心外膜突破部位，局部纤维方向和BZ边缘之间的相互作用。