A Numerical Analysis of the Hemodynamic Functionality of Human Coronary Stenosis Under Different Physiologic Conditions and Boundary Condition Formulations
Abstract Coronary artery disease (CAD) is among the foremost causes for human death worldwide. This study aims at investigating the performance of different boundary condition model types to characterize CAD functional significance. In addition, alternate models to estimate FFR using any different combination of boundary conditions at inlet and outlet were analyzed. In the first type of boundary condition, an outflow resistance model is used combined with a fixed pressure at inlet. In the second model of boundary conditions, constant pressure values are imposed at the domain inlet and outlet/s sections. In the third model, a zero diffusion flux is applied at outlet with a pre-specified flow rate at inlet. Numerical simulations performed on healthy and stenosed idealized and physiological arterial models revealed the superiority of the first type of boundary condition to directly capture the level of ischemia in diseased arteries. However, in this model, special numerical treatment at the outflow boundary is needed to dampen pseudo numerical reflections entering the computational domain. Alternative simple methods are developed to tackle the problem incurred in the second and third types of boundary condition types. The alternate models are effective for carrying extensive parametric studies with minimal computational effort. The new developed methods allow results generated via generic simulations under any specified boundary condition type to correctly estimate CAD functional significance. The obtained surrogate models account for the effects of the patient-specific physiologic parameters and can be easily incorporated without modifying existing CFD codes. Moreover, where it is unfeasible to experimentally incorporate the downstream effects of a given diseased arterial segment, an important aspect the alternative models provide is that they can be easily adopted by experimentalists through building in-vitro arterial models to assess the functional significance of the obstruction caused by the disease and its relation to any given patient specific physiologic parameter.