When flow-induced forces are altered at the blood vessel, maladaptive remodeling can occur. One reason such remodeling may occur has to do with the abnormal functioning of the aortic heart valve due to disease, calcification, injury, or an improperly-designed prosthetic valve, which restricts the opening of the valve leaflets and drastically alters the hemodynamics in the ascending aorta. While the specifics underlying the fundamental mechanisms leading to changes in heart valve function may differ from one cause to another, one common and important change is in leaflet stiffness and/or mass. Here, we examine the link between valve stiffness and mass and the hemodynamic environment in aorta by coupling magnetic resonance imaging (MRI) with high-resolution fluid–structure interaction (FSI) computational fluid dynamics to simulate blood flow in a patient-specific model. The thoracic aorta and a native aortic valve were re-constructed in the FSI model from the MRI data and used for the simulations. The effect of valve stiffness and mass is parametrically investigated by varying the thickness (h) of the leaflets (h = 0.6, 2, 4 mm). The FSI simulations were designed to investigate systematically progressively higher levels of valve stiffness by increasing valve thickness and quantifying hemodynamic parameters known to be linked to aortopathy and valve disease. The computed results reveal dramatic differences in all hemodynamic parameters: (1) the geometric orifice area (GOA), (2) the maximum velocity V max of the jet passing through the aortic orifice area, (3) the rate of energy dissipation E ˙ diss ( t ) , (4) the total loss of energy E diss , (5) the kinetic energy of the blood flow E kin ( t ) , and (6) the average magnitude of vorticity Ω a ( t ) , illustrating the change in hemodynamics that occur due to the presence of aortic valve stenosis.
A simplified method to account for wall motion in patient-specific blood flow simulations of aortic dissection: Comparison with fluid-structure interaction
