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Constitutive Modeling of Cardiac Tissue Growth

机译:心脏组织生长的本构模型

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摘要

Long term responses of the heart to e.g. infarction or surgical intervention are related to response of the tissue to changes in the mechanical environment. The tissue response is likely to involve (local) change of mass. Implementation of the associated inhomogeneous change in volume for a complex geometry is cumbersome. In the present study, we propose a computational framework for finite volumetric growth. The local stimulus for growth is determined from a simulation of beat to beat cardiac mechanics, assuming the tissue to be incompressible. The related local volumetric growth is translated in a global change of cardiac shape through a simulation of long term cardiac mechanics, assuming the tissue to be compressible. We illustrate the model by simulating growth in response to a deviation of end-diastolic sarcomeric strain from a set optimal value assumed to be preferred by the tissue. Inhomogeneity in the stimulus was reduced after inhomogeneous growth of up to 25%. The transmural redistribution of mass due to growth was found to alter an initially unphysiological linear transmural course in myofiber orientations to a more physiological course. We conclude that the model enables simulation of locally inhomogeneous growth in a realistic left ventricular geometry.
机译:心脏对例如心脏的长期反应梗塞或手术干预与组织对机械环境变化的反应有关。组织反应可能涉及(局部)质量改变。对于复杂的几何体,相关的体积的不均匀变化的实现是麻烦的。在本研究中,我们提出了有限体积增长的计算框架。假设组织是不可压缩的,则通过逐次搏动心脏力学的模拟来确定用于生长的局部刺激。假设组织是可压缩的,则通过模拟长期心脏力学,可以将相关的局部体积增长转化为心脏形状的整体变化。我们通过模拟响应于舒张末期肌节肌张力与假定为组织优选的设定最佳值之间的偏差的增长来说明该模型。高达25%的不均匀生长后,刺激中的不均匀性降低了。发现由于生长引起的质量的透壁再分布将肌纤维取向的最初非生理性线性透壁过程改变为更生理的过程。我们得出的结论是,该模型能够模拟现实的左心室几何形状中的局部不均匀生长。

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