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。

本文旨在研究病理生理情况（例如心房颤动和急性二尖瓣反流）中肺血流动力学与左心功能之间的详细机械相互作用。这是通过为肺循环，左心房和二尖瓣模型耦合开发复杂的计算框架来实现的。左心房和二尖瓣采用生理学上逼真的三维几何形状，纤维增强的超弹性材料和流体-结构相互作用进行建模，肺血管建模为以结构化树为末端的一维网络，并具有特定的血管几何结构和壁材料特性。这个新的耦合模型揭示了一些有趣的结果，可能具有诊断价值。例如，通过肺血管的波传播会导致第二次收缩流波（S2波）在肺静脉之间的到达时间不同，从而在左心房内部形成涡流环。在急性二尖瓣关闭不全的情况下，左心房会增加能量耗散和压力升高。肺静脉可经历波强度增加，收缩期逆流和舒张早期血流波（D波）增加，进而引起二尖瓣横穿的另一波血流（L波），以及二尖瓣血流的逆流。左心耳孔。如果是房颤，我们发现主动收缩的丧失与左心耳内的血流较慢以及肺静脉中的舒张后期​​房性逆转波（AR波）和第一个收缩期波（S1波）的消失有关。从微观血管到主要肺动脉，沿着肺血管树的血流动力学变化在不同的尺度上都可以在该模型中捕获。这项工作有望在量化疾病进展和各种肺部疾病（例如由于左心功能不全引起的肺动脉高压）的医学治疗方面发挥潜力。