右心室心肌被动力学行为的多尺度计算模型。

David S. Li, Emilio A. Mendiola, R. Avazmohammadi, F. Sachse, Michael S. Sacks
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引用次数: 1

摘要

我们之前已经证明了肌纤维-胶原力学相互作用在右心室游离壁(RVFW)心肌被动力学行为建模中的重要性。为了更深入地了解这些耦合机制,我们通过结合高分辨率成像和基于超级计算机的模拟,开发了高保真度、微观解剖逼真的右心室游离壁(RVFW)心肌三维有限元模型。我们首先在亚组织尺度上建立了代表性组织元件(RTE)模型,专门研究了肌纤维和ECM胶原的超弹性各向异性结构本构关系,并利用开源软件FEniCS模拟了等双轴和非等双轴加载条件,计算了RTE的有效应力应变响应。为了估计RTE模型的模型参数,我们首先将“自上而下”的双轴应力-应变行为与我们之前基于结构(组织尺度)的模型相匹配,该模型由测量的肌纤维和胶原纤维组成和取向分布提供信息。接下来,我们采用多尺度方法通过“自下而上”的均质化拟合的RTE模型来确定组织水平(5 x 5 x 0.7 mm标本大小)RVFW双轴行为,将组织学测量的肌纤维和胶原取向概括为双轴力学数据。我们的均质化方法成功再现了我们之前研究中所有双轴变形模式下的组织水平力学行为,这表明肌纤维和ECM胶原的三维微观解剖安排确实是驱动肌纤维-胶原相互作用的主要机制。
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A multi-scale computational model for the passive mechanical behavior of right ventricular myocardium.
We have previously demonstrated the importance of myofiber-collagen mechanical interactions in modeling the passive mechanical behavior of right ventricle free wall (RVFW) myocardium. To gain deeper insights into these coupling mechanisms, we developed a high-fidelity, micro-anatomically realistic 3D finite element model of right ventricle free wall (RVFW) myocardium by combining high-resolution imaging and supercomputer-based simulations. We first developed a representative tissue element (RTE) model at the sub-tissue scale by specializing the hyperelastic anisotropic structurally-based constitutive relations for myofibers and ECM collagen, and equi-biaxial and non-equibiaxial loading conditions were simulated using the open-source software FEniCS to compute the effective stress-strain response of the RTE. To estimate the model parameters of the RTE model, we first fitted a 'top-down' biaxial stress-strain behavior with our previous structurally based (tissue-scale) model, informed by the measured myofiber and collagen fiber composition and orientation distributions. Next, we employed a multi-scale approach to determine the tissue-level (5 x 5 x 0.7 mm specimen size) RVFW biaxial behavior via 'bottom-up' homogenization of the fitted RTE model, recapitulating the histologically measured myofiber and collagen orientation to the biaxial mechanical data. Our homogenization approach successfully reproduced the tissue-level mechanical behavior of our previous studies in all biaxial deformation modes, suggesting that the 3D micro-anatomical arrangement of myofibers and ECM collagen is indeed a primary mechanism driving myofiber-collagen interactions.
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