Fluid structure interaction modelling of aortic valve stenosis: Effects of valve calcification on coronary artery flow and aortic root hemodynamics.

BACKGROUND AND OBJECTIVE: Coronary artery diseases and aortic valve stenosis are two of the main causes of mortality and morbidity worldwide. Stenosis of the aortic valve develops due to calcium deposition on the aortic valve leaflets during the cardiac cycle. Clinical investigations have demonstrated that aortic valve stenosis not only affects hemodynamic parameters inside the aortic root but also has a significant influence on the coronary artery hemodynamics and leads to the initiation of coronary artery disease. The aim of this study is to investigate the effect of calcification of the aortic valve on the variation of hemodynamic parameters in the aortic root and coronary arteries in order to find potential locations for initiation of the coronary stenoses. METHODS: Fluid structure interaction modelling methodology was used to simulate aortic valve hemodynamics in the presence of coronary artery flow. A 2-D model of the aortic valve leaflets was developed in ANSYS Fluent based on the available echocardiography images in literature. The k-ω SST turbulence model was utilised to model the turbulent flow downstream of the leaflets. RESULTS: The effects of calcification of the aortic valve on aortic root hemodynamics including transvalvular pressure gradient, valve orifice dimeter, vorticity magnitude in the sinuses and wall shear stress on the ventricularis and fibrosa layers of the leaflets were studied. Results revealed that the transvalvular pressure gradient increases from 792 Pa (∼ 6 mmHg) for a healthy aortic valve to 2885 Pa (∼ 22 mmHg) for a severely calcified one. Furthermore, the influence of the calcification of the aortic valve leaflets on the velocity profile and the wall shear stress in the coronary arteries was investigated and used for identification of potential locations of initiation of the coronary stenoses. Obtained results show that the maximum velocity inside the coronary arteries at early diastole decreases from 1 m/s for the healthy valve to 0.45 m/s for the severely calcified case. CONCLUSIONS: Calcification significantly decreases the wall shear stress of the coronary arteries. This reduction in the wall shear stress can be a main reason for initiation of the coronary atherosclerosis process and eventually results in coronary stenoses.

Transitional turbulent flow in a stenosed coronary artery with a physiological pulsatile flow.

The turbulence in the blood flow, caused by plaque deposition on the arterial wall, increases by the combined effect of the complex plaque geometries and the pulsatile blood flow. The correlation between the plaque geometry, the pulsatile inlet flow and the induced turbulence in a constricted artery is investigated in this study. Pressure drop, flow velocity and wall shear stress are determined for stenosed coronary artery models with three different degrees of asymmetric stenosis and for different heart working conditions. A Computational Fluid Dynamics model, validated against experimental data published in the literature, was developed to simulate the blood pulsatile flow inside a stenosed coronary artery model. The transitional flow behaviour was quantified by investigation of the changes in the turbulence kinetic energy. It was shown that the separation starts from the side of the asymmetric stenosis and spreads to its opposite side further downstream. The results suggest that there is a high risk of the formation of a secondary stenosis at a downstream distance equal to 10 times of the artery diameter at the side and bottom regions of the first stenosis due to the existence of the recirculation zones and low shear stresses. Finally, a stenosed patient-specific coronary artery model was employed to illustrate the applicability of the obtained results for real geometry models. The results of this study provide a good prediction of pressure drop and blood flow rate, which can be applied in the investigation of the heart muscle workout and the required heart power.