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

Fluid-structure interaction in a fully coupled three-dimensional mitral-atrium-pulmonary model.
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DOI:
10.1007/s10237-021-01444-6
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发表时间:
2021-08
影响因子:
3.5
通讯作者:
Luo X
Luo X
中科院分区:
工程技术2区
文献类型:
--
作者:
Feng L;Gao H;Qi N;Danton M;Hill NA;Luo X

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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(例如房颤和急性二尖瓣返流)之间的详细机械相互作用。这是通过开发一个复杂的计算框架耦合肺循环,左心房和二尖瓣模型。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束的一维网络,具有指定的血管几何形状和壁材料特性。这个新的耦合模型揭示了一些有趣的结果,可能是诊断价值。例如,通过肺脉管系统的波传播可以导致肺静脉之间的第二收缩流波(S2波)的不同到达时间,从而在左心房内形成涡环。在急性二尖瓣返流的情况下,左心房经历增加的能量耗散和压力升高。肺静脉可经历增加的波强度、收缩期间的反向流动和增加的舒张早期流动波(D波),这进而引起穿过二尖瓣的附加流动波(L波)以及左心耳口处的反向流动。在心房颤动的情况下,我们发现,主动收缩的损失与左心耳内的血流减慢和肺静脉中的晚期心房逆转波(AR波)和第一收缩波(S1波)的消失有关。该模型可以捕捉到肺血管树沿着从微观血管到主肺动脉的不同尺度的血流动力学变化。这项工作有望在量化疾病进展和各种肺部疾病的医学治疗,如由于左心功能不全的肺动脉高压。
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.
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