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Fluid-structure interaction in a fully coupled three-dimensional mitral-atrium-pulmonary model

机译:完全耦合的三维二核 - 肺模型中的流体结构相互作用

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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.
机译:本文旨在探讨肺部血管动力学与病理生理情况(例如心房颤动和急性二尖瓣急性反流的左心功能之间的详细机械相互作用。这是通过开发用于耦合肺循环,左心房和二尖瓣模型的复杂计算框架来实现的。左心房和二尖瓣均采用生理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,并且肺部血管被建模为一维网络以结构树木结束,具有指定的船舶几何形状和墙壁材料特性。该新耦合模型揭示了一些可能具有诊断价值的有趣结果。例如,通过肺脉管系统的波传播可以导致肺静脉中的第二收缩波(S2波)的不同到达时间,在左心房内形成涡旋环。在急性二尖瓣反流的情况下,左心房经历了增加的能量耗散和压力升高。肺静脉可以体验增加的波浪强度,在收缩过程中的逆转流动和增加的早期舒张流流浪波(D波),这反过来导致二尖瓣(L波)的额外流浪,以及逆转流动左心房阑尾孔。在心房颤动的情况下,我们表明活跃收缩的损失与左心房阑尾和后期心房逆转波(AR波)的左心房阑尾和失踪和第一个收缩波(S1波)内的较慢流动相关肺静脉。沿着肺部血管树木的血管血管血管从来自微观血管与主要肺动脉的肺部血管树木的变化都可以在该模型中捕获。该作品承诺对由于左心功能障碍而定量疾病进展和各种肺病等肺部疾病的医疗治疗的潜力。

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