Department of Biomedical Engineering, Eindhoven University of Technology, 5600MB, Eindhoven, The Netherlands.
Biomech Model Mechanobiol. 2024 Dec;23(6):1963-1976. doi: 10.1007/s10237-024-01877-9. Epub 2024 Aug 1.
Acute myocardial infarction (MI) leads to a loss of cardiac function which, following adverse ventricular remodeling (AVR), can ultimately result in heart failure. Tissue-engineered contractile patches placed over the infarct offer potential for restoring cardiac function and reducing AVR. In this computational study, we investigate how improvement of pump function depends on the orientation of the cardiac patch and the fibers therein relative to the left ventricle (LV). Additionally, we examine how model outcome depends on the choice of material properties for healthy and infarct tissue. In a finite element model of LV mechanics, an infarction was induced by eliminating active stress generation and increasing passive tissue stiffness in a region comprising 15% of the LV wall volume. The cardiac patch was modeled as a rectangular piece of healthy myocardium with a volume of 25% of the infarcted tissue. The orientation of the patch was varied from 0 to relative to the circumferential plane. The infarct reduced stroke work by 34% compared to the healthy heart. Optimal patch support was achieved when the patch was oriented parallel to the subepicardial fiber direction, restoring 9% of lost functionality. Typically, about one-third of the total recovery was attributed to the patch, while the remainder resulted from restored functionality in native myocardium adjacent to the infarct. The patch contributes to cardiac function through two mechanisms. A contribution of tissue in the patch and an increased contribution of native tissue, due to favorable changes in mechanical boundary conditions.
急性心肌梗死 (MI) 导致心脏功能丧失,随后发生不良心室重构 (AVR),最终导致心力衰竭。在梗死部位放置组织工程收缩性贴片有望恢复心脏功能并减少 AVR。在这项计算研究中,我们研究了泵功能的改善如何取决于心脏贴片的方向以及相对于左心室 (LV) 的贴片内的纤维。此外,我们还研究了模型结果如何取决于健康和梗死组织的材料特性选择。在 LV 力学的有限元模型中,通过消除主动应力产生并增加 LV 壁体积的 15%区域中的被动组织刚度来诱导梗死。将心脏贴片建模为健康心肌的矩形片,其体积为梗死组织的 25%。贴片的方向从 0 变化到相对于环面的 。与健康心脏相比,梗死使冲程功减少了 34%。当贴片与心外膜纤维方向平行定向时,贴片可提供最佳支撑,恢复了 9%的丧失功能。通常,总恢复量的约三分之一归因于贴片,而其余部分归因于梗死附近固有心肌的恢复功能。贴片通过两种机制对心脏功能做出贡献。贴片中的组织和由于机械边界条件的有利变化而增加的固有组织的贡献。