心脏双心室电动力学仿真的3D-0 D闭环模型
3D-0D closed-loop model for the simulation of cardiac biventricular electromechanics
摘要：
心脏电动力学的精确数值模拟的两个关键因素（其对于再现心脏的同步活动也是必不可少的）是：i）考虑心脏和循环系统之间的相互作用，其确定心腔中的压力和容积负荷; ii）重建驱动电生理信号和心肌收缩的肌肉纤维结构。在这项工作中，我们提出了一个三维双心室机电模型，加上一个0 D闭环模型的整个心血管系统，解决了前两个关键因素。有了这个目的，我们引入了一个边界条件的机械问题，占被忽视的部分域位于顶部的双心室基底平面，这是一致的动量和能量守恒的原则。我们还详细讨论了3D和0 D模型背后的耦合条件。我们使用3D-0 D模型在生理条件下进行机电模拟，结果表明我们的结果与文献中相关机械生物标志物的实验数据相匹配。此外，我们还研究了交叉纤维主动收缩的不同排列方式。我们证明了一个积极的张力沿片方向抵消肌纤维收缩，而一个沿片法线方向增强心脏的工作。最后，分析了几种肌纤维结构。我们发现，不同的纤维领域中的间隔区和透壁影响左心室的泵功能。
英文摘要：
Two crucial factors for accurate numerical simulations of cardiac electromechanics, which are also essential to reproduce the synchronous activity of the heart, are: i) accounting for the interaction between the heart and the circulatory system that determines pressures and volumes loads in the heart chambers; ii) reconstructing the muscular fiber architecture that drives the electrophysiology signal and the myocardium contraction. In this work, we present a 3D biventricular electromechanical model coupled with a 0D closed-loop model of the whole cardiovascular system that addresses the two former crucial factors. With this aim, we introduce a boundary condition for the mechanical problem that accounts for the neglected part of the domain located on top of the biventricular basal plane and that is consistent with the principles of momentum and energy conservation. We also discuss in detail the coupling conditions that stand behind the 3D and the 0D models. We perform electromechanical simulations in physiological conditions using the 3D-0D model and we show that our results match the experimental data of relevant mechanical biomarkers available in literature. Furthermore, we investigate different arrangements in cross-fibers active contraction. We prove that an active tension along the sheet direction counteracts the myofiber contraction, while the one along the sheet-normal direction enhances the cardiac work. Finally, several myofiber architectures are analysed. We show that a different fiber field in the septal area and in the transmural wall effect the pumping functionality of the left ventricle.
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