A Micro-anatomical Model of the Infarcted Left Ventricle Border Zone to Study the Influence of Collagen Undulation.

Emilio A Mendiola, Eric Wang, Abby Leatherman, Qian Xiang, Sunder Neelakantan, Peter Vanderslice, Reza Avazmohammadi
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Abstract

Myocardial infarction (MI) results in cardiac myocyte death and often initiates the formation of a fibrotic scar in the myocardium surrounded by a border zone. Myocyte loss and collagen-rich scar tissue heavily influence the biomechanical behavior of the myocardium which could lead to various cardiac diseases such as systolic heart failure and arrhythmias. Knowledge of how myocyte and collagen micro-architecture changes affect the passive mechanical behavior of the border zone remains limited. Computational modeling provides us with an invaluable tool to identify and study the mechanisms driving the biomechanical remodeling of the myocardium post-MI. We utilized a rodent model of MI and an image-based approach to characterize the three-dimensional (3-D) myocyte and collagen micro-architecture at various timepoints post-MI. Left ventricular free wall (LVFW) samples were obtained from infarcted hearts at 1-week and 4-week post-MI (n = 1 each). Samples were labeled using immunoassays to identify the extracellular matrix (ECM) and myocytes. 3-D reconstructions of the infarct border zone were developed from confocal imaging and meshed to develop high-fidelity micro-anatomically accurate finite element models. We performed a parametric study using these models to investigate the influence of collagen undulation on the passive micromechanical behavior of the myocardium under a diastolic load. Our results suggest that although parametric increases in collagen undulation elevate the strain amount experienced by the ECM in both early- and late-stage MI, the sensitivity of myocytes to such increases is reduced from early to late-stage MI. Our 3-D micro-anatomical modeling holds promise in identifying mechanisms of border zone maladaptation post-MI.

研究胶原褶皱影响的左心室梗死边界区微型解剖模型
心肌梗塞(MI)会导致心肌细胞死亡,通常会在心肌中形成纤维化瘢痕,周围形成边界区。心肌细胞的丧失和富含胶原蛋白的瘢痕组织严重影响心肌的生物力学行为,从而导致各种心脏疾病,如收缩性心力衰竭和心律失常。关于心肌细胞和胶原微结构变化如何影响边界区被动机械行为的知识仍然有限。计算建模为我们提供了一种宝贵的工具,可用于识别和研究心肌梗死后心肌生物力学重塑的驱动机制。我们利用啮齿动物心肌梗死模型和基于图像的方法来描述心肌梗死后不同时间点的三维(3-D)心肌细胞和胶原微结构。从心肌梗死后 1 周和 4 周的梗死心脏中获取左心室游离壁 (LVFW) 样本(n = 1)。使用免疫测定法对样本进行标记,以识别细胞外基质(ECM)和心肌细胞。通过共焦成像对梗死边缘区进行三维重建,并将其网格化,以建立高保真微解剖精确有限元模型。我们利用这些模型进行了参数研究,以探讨胶原起伏对心肌在舒张负荷下被动微观力学行为的影响。我们的研究结果表明,虽然胶原起伏的参数化增加会使早期和晚期心肌梗死中 ECM 所承受的应变量增加,但从早期到晚期心肌梗死,心肌细胞对这种增加的敏感性会降低。我们的三维微解剖建模有望确定心肌梗死后边缘区适应不良的机制。
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