Hemodynamics of a stenosed aortic valve: Effects of the geometry of the sinuses and the positions of the coronary ostia

Abstract

Aortic valve stenosis is one of the most prevalent cardiovascular disease among adults worldwide. Stenosis of the aortic valve changes the hemodynamic parameters inside the aortic root which perpetuates aortic valve calcification and has been associated with the development of coronary artery atherosclerosis. Invasive studies have revealed that the geometry of the sinuses, as well as the locations of the coronary artery ostia, impact coronary blood flow hemodynamics, which has been associated with the development of coronary artery disease. The aim of this study is to elucidate this observed phenomenon, in which geometrical variations inside the aortic root and malfunctioning of the aortic valve because of the calcification not only affect the progression of the calcification but also lead to initiation of coronary artery atherosclerosis. A 2D fluid structure interaction model of the aortic valve was developed and simulated in ANSYS Fluent based on available echocardiography images in the literature. The model incorporates fluid structure interaction and employs the k − ω Menter's Shear Stress Transport (SST) turbulence model for the turbulent flow downstream of the leaflets. The effects of various diameters of the sinuses 25, 20.8, and 17.6 mm and positions of the coronary artery ostia (proximal, middle, and distal) on aortic root hemodynamics were investigated and parameters including transvalvular pressure gradient, valve orifice diameters, maximum jet velocity along the valve orifice area, and wall shear stresses on leaflets calculated. Results demonstrate that a severely calcified valve with the proximal coronary artery ostia witnesses a much higher transvalvular pressure gradient (approximately 10 times larger) compared to that for a healthy case. Moreover, the presence of the proximal coronary artery ostia for valves with diameters of the sinus 25 and 20.8 mm results in the reduction of the coronary blood flow and increase of the probability of coronary artery atherosclerosis.