ArticleBiomechanics and modeling in mechanobiology2021
Fluid-structure interaction in a fully coupled three-dimensional mitral-atrium-pulmonary model.
Article in Biomechanics and modeling in mechanobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 16 citations in OpenAlex.
- Toward precision in simulation of paediatric mitral valve repair using patient-specific fluid-structure interaction modelling.European heart journal. Imaging methods and practice · 2026Article
- Three-dimensional fluid-structure interaction modelling of the venous valve using immersed boundary/finite element method.Computers in biology and medicine · 2025Article
- Efficient uncertainty quantification in a spatially multiscale model of pulmonary arterial and venous hemodynamics.Biomechanics and modeling in mechanobiology · 2024Article
- Increased Blood Residence Time as Markers of High-Risk Patent Foramen Ovale.Translational stroke research · 2023Article
- Subject-specific factors affecting particle residence time distribution of left atrial appendage in atrial fibrillation: A computational model-based study.Frontiers in cardiovascular medicine · 2023Article
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Authors and funding
6 authors at 3 institutions in 2 countries.
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Abstract
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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