一种用于整个人体心脏仿真的电机械驱动流体动力学模型
An electromechanics-driven fluid dynamics model for the simulation of the whole human heart
AI总结：
本文构建由四腔电机械模型驱动的整心多物理场多尺度 CFD 模型，经 RDQ20 校准后可定量再现生理与左束支传导阻滞病理血流动力学。
摘要：
我们提出了一种多物理场和几何多尺度计算模型，适用于描述由四腔电机械模型驱动的整个人体心脏的血流动力学。我们首先展示了一项关于生物物理细节丰富的 RDQ20 激活模型（Regazzoni 等人，2020）校准的研究，该模型能够再现血流动力学生物标志物的生理范围。随后，我们证明，力生成模型再现某些微观尺度机制的能力——例如力对肌纤维缩短速度的依赖性——对于捕捉整体生理性的力学与流体动力学宏观尺度行为至关重要。这表明，即使关注的输出与宏观尺度相关，也有必要使用具有高生物物理保真度的多尺度模型。我们表明，使用高保真电机械模型并结合细致的校准过程，使我们能够在力学量和血流动力学量两方面实现显著的生物物理保真度。事实上，我们在解剖学精确的整个心脏几何结构上开展的电机械驱动 CFD 模拟，给出了在定性（就流动模式而言）和定量（将在硅结果与体内获取的生物标志物进行比较时）两方面均与心脏生理相匹配的结果。我们考虑左束支传导阻滞这一病理病例，并借助我们的多物理场集成模型研究电异常对心脏血流动力学产生的后果。我们提出的计算模型能够忠实预测病理条件下左心室中的延迟以及不断增加的壁面剪应力。不同物理过程在集成框架中的相互作用，使我们能够通过捕捉和再现人类心脏内在的多物理场本质，忠实描述并建模这种病理。
英文摘要：
We introduce a multiphysics and geometric multiscale computational model, suitable to describe the hemodynamics of the whole human heart, driven by a four-chamber electromechanical model. We first present a study on the calibration of the biophysically detailed RDQ20 activation model (Regazzoni et al., 2020) that is able to reproduce the physiological range of hemodynamic biomarkers. Then, we demonstrate that the ability of the force generation model to reproduce certain microscale mechanisms, such as the dependence of force on fiber shortening velocity, is crucial to capture the overall physiological mechanical and fluid dynamics macroscale behavior. This motivates the need for using multiscale models with high biophysical fidelity, even when the outputs of interest are relative to the macroscale. We show that the use of a high-fidelity electromechanical model, combined with a detailed calibration process, allows us to achieve remarkable biophysical fidelity in terms of both mechanical and hemodynamic quantities. Indeed, our electromechanical-driven CFD simulations - carried out on an anatomically accurate geometry of the whole heart - provide results that match the cardiac physiology both qualitatively (in terms of flow patterns) and quantitatively (when comparing in silico results with biomarkers acquired in vivo). We consider the pathological case of left bundle branch block, and we investigate the consequences that an electrical abnormality has on cardiac hemodynamics thanks to our multiphysics integrated model. The computational model that we propose can faithfully predict a delay and an increasing wall shear stress in the left ventricle in the pathological condition. The interaction of different physical processes in an integrated framework allows us to faithfully describe and model this pathology, by capturing and reproducing the intrinsic multiphysics nature of the human heart.
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