Three-dimensional structural analysis of double-entry and single-entry coal mines. Final report. Vol 2. Users guide for a computer program for analytical modelling of rock-structure interaction

AbstractThis 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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Modeling of aortic valve stenosis using fluid-structure interaction method

Perfusion ◽

10.1177/0267659121998549 ◽

2021 ◽

pp. 026765912199854

Author(s):

Mohammad Javad Ghasemi Pour ◽

Kamran Hassani ◽

Morteza Khayat ◽

Shahram Etemadi Haghighi

Keyword(s):

Blood Flow ◽

Aortic Valve ◽

Fluid Structure Interaction ◽

Three Dimensional ◽

Fluid Structure ◽

Structure Interaction ◽

Relaxation Phase ◽

Exercise Condition ◽

Time Dependent Domain ◽

Comparison Of The Results

Background and objectives: Fluid structure interaction (FSI) is defined as interaction of the structures with contacting fluids. The aortic valve experiences the interaction with blood flow in systolic phase. In this study, we have tried to predict the hemodynamics of blood flow through a normal and stenotic aortic valve in two relaxation and exercise conditions using a three-dimensional FSI method. Methods: The aorta valve was modeled as a three-dimensional geometry including a normal model and two others with 25% and 50% stenosis. The geometry of the aortic valve was extracted from CT images and the models were generated by MMIMCS software and then they were implemented in ANSYS software. The pulsatile flow rate was used for all cases and the numerical simulations were conducted based on a time-dependent domain. Results: The obtained results including the velocity, pressure, and shear stress contours in different systolic time sequences were explained and discussed. The maximum blood flow velocity in relaxation phase was obtained 1.62 m/s (normal valve), 3.78 m/s (25% stenosed valve), and 4.73 m/s (50% stenosed valve). In exercise condition, the maximum velocities are 2.86, 4.32, and 5.42 m/s respectively. The maximum blood pressure in relaxation phase was calculated 111.45 mmHg (normal), 148.66 mmHg (25% stenosed), and 164.21 mmHg (50% stenosed). However, the calculated values in exercise situation were 129.57, 163.58, and 191.26 mmHg. The validation of the predicted results was also conducted using existing literature. Conclusions: We believe that such model are useful tools for biomechanical experts. The further studies should be done using experimental data and the data are implemented on the boundary conditions for better comparison of the results.

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