School of Mathematics and Statistics, University of Glasgow, Glasgow, G12 8SQ, UK.
Institute of Marine Science and Technology, Shandong University, Shangdong, 266237, People's Republic of China.
Biomech Model Mechanobiol. 2021 Aug;20(4):1267-1295. doi: 10.1007/s10237-021-01444-6. Epub 2021 Mar 26.
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.
本文旨在研究病理生理情况下（如心房颤动和急性二尖瓣反流）肺血液动力学与左心功能之间的详细力学相互作用。这是通过开发一个用于耦合肺循环、左心房和二尖瓣模型的复杂计算框架来实现的。左心房和二尖瓣采用具有生理现实性的三维几何形状、纤维增强超弹性材料和流固耦合进行建模，肺血管采用一维网络建模，网络末端为结构化树，指定了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可能具有诊断价值的有趣结果。例如，波在肺脉管系统中的传播会导致肺静脉中第二个收缩波（S2 波）的到达时间不同，从而在左心房内形成涡环。在急性二尖瓣反流的情况下，左心房经历能量耗散和压力升高的增加。肺静脉可能会经历更高的波强度、收缩期反流和早期舒张波（D 波）的增加，这反过来又会导致二尖瓣（L 波）上的额外流动波以及左心房附壁开口处的反流。在心房颤动的情况下，我们表明主动收缩的丧失与左心房附壁内的血流速度减慢有关，并且肺静脉中的晚期舒张期心房反流波（AR 波）和第一收缩波（S1 波）消失。在不同尺度（从微观血管到主肺动脉）的肺血管树中，都可以捕捉到这种模型中的血流动力学变化。这项工作有望在量化各种肺部疾病（如左心功能障碍引起的肺动脉高压）的疾病进展和医疗治疗方面具有潜力。
