School of Computer Science and Technology, Harbin Institute of Technology (HIT), Harbin, China.
Peng Cheng Laboratory, Shenzhen, China.
PLoS Comput Biol. 2022 Apr 27;18(4):e1009388. doi: 10.1371/journal.pcbi.1009388. eCollection 2022 Apr.
Myocardial ischemia, injury and infarction (MI) are the three stages of acute coronary syndrome (ACS). In the past two decades, a great number of studies focused on myocardial ischemia and MI individually, and showed that the occurrence of reentrant arrhythmias is often associated with myocardial ischemia or MI. However, arrhythmogenic mechanisms in the tissue with various degrees of remodeling in the ischemic heart have not been fully understood. In this study, biophysical detailed single-cell models of ischemia 1a, 1b, and MI were developed to mimic the electrophysiological remodeling at different stages of ACS. 2D tissue models with different distributions of ischemia and MI areas were constructed to investigate the mechanisms of the initiation of reentrant waves during the progression of ischemia. Simulation results in 2D tissues showed that the vulnerable windows (VWs) in simultaneous presence of multiple ischemic conditions were associated with the dynamics of wave propagation in the tissues with each single pathological condition. In the tissue with multiple pathological conditions, reentrant waves were mainly induced by two different mechanisms: one is the heterogeneity along the excitation wavefront, especially the abrupt variation in conduction velocity (CV) across the border of ischemia 1b and MI, and the other is the decreased safe factor (SF) for conduction at the edge of the tissue in MI region which is attributed to the increased excitation threshold of MI region. Finally, the reentrant wave was observed in a 3D model with a scar reconstructed from MRI images of a MI patient. These comprehensive findings provide novel insights for understanding the arrhythmic risk during the progression of myocardial ischemia and highlight the importance of the multiple pathological stages in designing medical therapies for arrhythmias in ischemia.
心肌缺血、损伤和梗死(MI)是急性冠状动脉综合征(ACS)的三个阶段。在过去的二十年中,大量研究集中在心肌缺血和 MI 上,结果表明折返性心律失常的发生通常与心肌缺血或 MI 有关。然而,在缺血心脏中具有不同程度重构的组织中的致心律失常机制尚未完全了解。在这项研究中,开发了缺血 1a、1b 和 MI 的生物物理详细单细胞模型,以模拟 ACS 不同阶段的电生理重构。构建了具有不同缺血和 MI 区域分布的 2D 组织模型,以研究在缺血进展过程中折返波起始的机制。2D 组织中的模拟结果表明,同时存在多种缺血条件下的脆弱窗口(VW)与组织中每种单一病理条件下波传播的动力学有关。在具有多种病理条件的组织中,折返波主要由两种不同的机制引起:一种是沿兴奋波前的异质性,特别是在缺血 1b 和 MI 的边界处传导速度(CV)的突然变化,另一种是在 MI 区域的组织边缘处传导的安全系数(SF)降低,这归因于 MI 区域的兴奋阈值增加。最后,在从 MI 患者的 MRI 图像重建的瘢痕 3D 模型中观察到折返波。这些综合发现为理解心肌缺血进展过程中的心律失常风险提供了新的见解,并强调了在设计缺血性心律失常治疗方案时多个病理阶段的重要性。