Impact of cardiac patch alignment on restoring post-infarct ventricular function

IF 3 3区 医学 Q2 BIOPHYSICS Biomechanics and Modeling in Mechanobiology Pub Date : 2024-08-01 DOI:10.1007/s10237-024-01877-9
Koen L. P. M. Janssens, Peter H. M. Bovendeerd
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Abstract

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 \(150^ \circ \) 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.

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心脏贴片排列对恢复梗死后心室功能的影响
急性心肌梗死(MI)会导致心脏功能丧失,在心室重塑(AVR)不良后,最终会导致心力衰竭。将组织工程收缩补片置于心肌梗死处,可恢复心脏功能并减少心室重构。在这项计算研究中,我们探讨了泵功能的改善如何取决于心脏补片及其纤维相对于左心室(LV)的方向。此外,我们还研究了模型结果如何取决于健康组织和梗塞组织的材料特性选择。在左心室力学有限元模型中,通过消除主动应力生成和增加占左心室壁体积 15%的区域的被动组织刚度来诱导梗塞。心脏补片被模拟为一块长方形的健康心肌,其体积为梗死组织的 25%。心肌补片的方向相对于圆周平面从 0 ∘ 到 150 ∘ 不等。与健康心脏相比,梗塞使卒中功减少了 34%。当补片的方向与心外膜下纤维方向平行时,可获得最佳的补片支持,恢复了 9% 丧失的功能。通常情况下,总恢复量的约三分之一归功于补片,而其余部分则来自于梗死邻近的原生心肌功能的恢复。补片通过两种机制促进心脏功能。一是补片中组织的贡献,二是由于机械边界条件的有利变化而增加了原生组织的贡献。
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来源期刊
Biomechanics and Modeling in Mechanobiology
Biomechanics and Modeling in Mechanobiology 工程技术-工程:生物医学
CiteScore
7.10
自引率
8.60%
发文量
119
审稿时长
6 months
期刊介绍: Mechanics regulates biological processes at the molecular, cellular, tissue, organ, and organism levels. A goal of this journal is to promote basic and applied research that integrates the expanding knowledge-bases in the allied fields of biomechanics and mechanobiology. Approaches may be experimental, theoretical, or computational; they may address phenomena at the nano, micro, or macrolevels. Of particular interest are investigations that (1) quantify the mechanical environment in which cells and matrix function in health, disease, or injury, (2) identify and quantify mechanosensitive responses and their mechanisms, (3) detail inter-relations between mechanics and biological processes such as growth, remodeling, adaptation, and repair, and (4) report discoveries that advance therapeutic and diagnostic procedures. Especially encouraged are analytical and computational models based on solid mechanics, fluid mechanics, or thermomechanics, and their interactions; also encouraged are reports of new experimental methods that expand measurement capabilities and new mathematical methods that facilitate analysis.
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