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Tachycardia in Post-Infarction Hearts: Insights from 3D Image-Based Ventricular Models

机译:梗死后心脏的心动过速:基于3D图像的心室模型的见解

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摘要

Ventricular tachycardia, a life-threatening regular and repetitive fast heart rhythm, frequently occurs in the setting of myocardial infarction. Recently, the peri-infarct zones surrounding the necrotic scar (termed gray zones) have been shown to correlate with ventricular tachycardia inducibility. However, it remains unknown how the latter is determined by gray zone distribution and size. The goal of this study is to examine how tachycardia circuits are maintained in the infarcted heart and to explore the relationship between the tachycardia organizing centers and the infarct gray zone size and degree of heterogeneity. To achieve the goals of the study, we employ a sophisticated high-resolution electrophysiological model of the infarcted canine ventricles reconstructed from imaging data, representing both scar and gray zone. The baseline canine ventricular model was also used to generate additional ventricular models with different gray zone sizes, as well as models in which the gray zone was represented as different heterogeneous combinations of viable tissue and necrotic scar. The results of the tachycardia induction simulations with a number of high-resolution canine ventricular models (22 altogether) demonstrated that the gray zone was the critical factor resulting in arrhythmia induction and maintenance. In all models with inducible arrhythmia, the scroll-wave filaments were contained entirely within the gray zone, regardless of its size or the level of heterogeneity of its composition. The gray zone was thus found to be the arrhythmogenic substrate that promoted wavebreak and reentry formation. We found that the scroll-wave filament locations were insensitive to the structural composition of the gray zone and were determined predominantly by the gray zone morphology and size. The findings of this study have important implications for the advancement of improved criteria for stratifying arrhythmia risk in post-infarction patients and for the development of new approaches for determining the ablation targets of infarct-related tachycardia.
机译:心室性心动过速是危及生命的规律性且反复性的快速心律,经常发生在心肌梗塞的环境中。最近,坏死疤痕周围的梗塞周围区域(称为灰色区域)已显示出与室性心动过速的诱导能力相关。但是,仍然不清楚如何通过灰色区域分布和大小确定后者。这项研究的目的是检查在梗塞的心脏中如何维持心动过速,并探讨心动过速组织中心与梗塞灰色区大小和异质程度之间的关系。为了达到研究的目的,我们采用了复杂的高分辨率电生理模型,通过成像数据重建了梗死的犬脑室,该模型既代表疤痕又代表灰色区域。基线犬心室模型还用于生成具有不同灰色区域大小的其他心室模型,以及其中灰色区域表示为活组织和坏死疤痕的不同异构组合的模型。许多高分辨率犬心室模型(共22个)的心动过速诱导模拟结果表明,灰色区域是导致心律不齐诱导和维持的关键因素。在所有可诱发的心律失常模型中,涡旋波丝完全包含在灰色区域内,无论其大小或成分的异质性水平如何。因此发现灰色区域是促心律失常的底物,其促进了波的破裂和折返形成。我们发现涡旋波丝的位置对灰色区域的结构组成不敏感,并且主要由灰色区域的形态和大小决定。这项研究的发现对提高梗死后患者心律失常危险分层标准的改进和确定梗死相关心动过速消融目标新方法的开发具有重要意义。

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