This paper aims to investigate detailed mechanical interactions between the pulmonary haemodynamics and left heart function in pathophysiological situations (e.g. atrial fibrillation and acute mitral regurgitation). This is achieved by developing a complex computational framework for a coupled pulmonary circulation, left atrium and mitral valve model. The left atrium and mitral valve are modelled with physiologically realistic three-dimensional geometries, fibre-reinforced hyperelastic materials and fluid-structure interaction, and the pulmonary vessels are modelled as one-dimensional network ended with structured trees, with specified vessel geometries and wall material properties. This new coupled model reveals some interesting results which could be of diagnostic values. For example, the wave propagation through the pulmonary vasculature can lead to different arrival times for the second systolic flow wave (S2 wave) among the pulmonary veins, forming vortex rings inside the left atrium. In the case of acute mitral regurgitation, the left atrium experiences an increased energy dissipation and pressure elevation. The pulmonary veins can experience increased wave intensities, reversal flow during systole and increased early-diastolic flow wave (D wave), which in turn causes an additional flow wave across the mitral valve (L wave), as well as a reversal flow at the left atrial appendage orifice. In the case of atrial fibrillation, we show that the loss of active contraction is associated with a slower flow inside the left atrial appendage and disappearances of the late-diastole atrial reversal wave (AR wave) and the first systolic wave (S1 wave) in pulmonary veins. The haemodynamic changes along the pulmonary vessel trees on different scales from microscopic vessels to the main pulmonary artery can all be captured in this model. The work promises a potential in quantifying disease progression and medical treatments of various pulmonary diseases such as the pulmonary hypertension due to a left heart dysfunction.

中文翻译：

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完全耦合的三维二尖瓣-心房-肺模型中的流体-结构相互作用。

本文旨在研究肺血流动力学和左心功能在病理生理情况下（例如心房颤动和急性二尖瓣关闭不全）之间的详细机械相互作用。这是通过为耦合肺循环、左心房和二尖瓣模型开发复杂的计算框架来实现的。左心房和二尖瓣采用生理上逼真的 3D 几何形状、纤维增强超弹性材料和流体-结构相互作用建模，肺血管建模为以结构化树结尾的一维网络，具有特定的血管几何形状和壁材料特性。这种新的耦合模型揭示了一些可能具有诊断价值的有趣结果。例如，波通过肺脉管系统传播可导致肺静脉中第二个收缩期血流波（S2 波）的到达时间不同，在左心房内形成涡环。在急性二尖瓣关闭不全的情况下，左心房经历增加的能量耗散和压力升高。肺静脉可能会经历波强度增加、收缩期逆流和舒张早期血流波（D 波）增加，这反过来会导致额外的流波穿过二尖瓣（L 波），以及在左心耳孔。在心房颤动的情况下，我们表明，主动收缩的丧失与左心耳内的较慢血流以及肺静脉中舒张晚期心房逆转波（AR 波）和第一收缩波（S1 波）的消失有关。从微观血管到主肺动脉的不同尺度的肺血管树的血流动力学变化都可以在该模型中捕捉到。这项工作有望量化疾病进展和各种肺部疾病的药物治疗，例如由左心功能障碍引起的肺动脉高压。