Janssens Koen L P M, Bovendeerd Peter H M
Department of Biomedical Engineering, Eindhoven University of Technology, Eindhoven 5600MB, The Netherlands.
Eindhoven University of Technology.
J Biomech Eng. 2025 Aug 1;147(8). doi: 10.1115/1.4068829.
Tissue-engineered contractile patches offer a promising therapeutic strategy to restore cardiac function following myocardial infarction (MI) and mitigate adverse ventricular remodeling, a key contributor to the progression of heart failure (HF). However, experimental and numerical studies indicate that their functionality may be affected by the mechanical properties of the underlying infarct. In this computational study, we investigate how infarct tissue stiffness and wall thickness influence the ability of a contractile cardiac patch to restore cardiac function. A model of cardiac mechanics was used to model MI in a region comprising 15% of the left ventricle. In this region, active stress generation was eliminated, and passive tissue stiffness and wall thickness were varied. The cardiac patch was modeled as a rectangular piece of healthy myocardium with a volume of 25% of the infarcted tissue. Following MI, stroke work decreased by 32% compared to the healthy heart. This loss increased with increasing infarct tissue stiffness and decreasing infarct wall thickness. In the most favorable case, the cardiac patch restored up to 15% of this loss, of which about one-third was attributed to a direct contribution of the patch and two-thirds to improved function in adjacent healthy myocardium. Decreasing tissue stiffness improved restoration of cardiac pump function and the relative contribution of the patch. Conversely, while reduced wall thickness improved restoration of pump function, it decreased the relative contribution of the patch. Lower infarct stiffness, either through tissue stiffness or wall thinning, allows more cardiac function to be restored via patch implantation.
组织工程收缩性补片为心肌梗死（MI）后恢复心脏功能及减轻不良心室重构提供了一种有前景的治疗策略，而不良心室重构是心力衰竭（HF）进展的关键因素。然而，实验和数值研究表明，其功能可能会受到梗死灶下方心肌机械性能的影响。在这项计算研究中，我们探究梗死组织硬度和壁厚如何影响收缩性心脏补片恢复心脏功能的能力。使用心脏力学模型对占左心室15%的区域进行MI建模。在该区域，消除主动应力生成，并改变被动组织硬度和壁厚。将心脏补片建模为一块健康心肌的矩形片，其体积为梗死组织的25%。MI后，与健康心脏相比，每搏功下降了32%。这种损失随着梗死组织硬度的增加和梗死壁厚的减小而增加。在最有利的情况下，心脏补片可恢复高达15%的这种损失，其中约三分之一归因于补片的直接作用，三分之二归因于相邻健康心肌功能的改善。降低组织硬度可改善心脏泵功能的恢复以及补片的相对作用。相反，虽然壁厚减小可改善泵功能的恢复，但会降低补片的相对作用。通过组织硬度降低或壁变薄实现的较低梗死硬度，可通过植入补片恢复更多的心脏功能。
