Non-Newtonian pulsatile blood flow through the stenosed arteries: comparison between the viscoelastic and elastic arterial wall in response to the alterations.

In this study, we investigate the impact of aortic stenosis on the hemodynamics of pulsatile blood flow within a 3D aortic model. Employing a non-Newtonian Casson model with a hematocrit of 45%, our study introduces a preliminary hypothesis to simulate blood flow dynamics, incorporating both linear elastic and viscoelastic models to define the mechanical characteristics of the artery. Through simulations conducted with Ansys-Cfx (version 15), we utilize a 2-way fluid-structure interaction (FSI) approach, employing a Lagrangian-Eulerian formulation with second-order accuracy. We explore the influence of stenosis severity on variables including velocity profiles, pressure distribution, shear stress, wall displacement, and changes in the OSI parameter. Our investigation encompasses arteries with both elastic and viscoelastic walls. The key findings that arise from our results highlight the viscoelastic model's demonstration of reduced radial wall displacement when compared to the linear elastic model. Additionally, we observe that elevated arterial stenosis percentages lead to the elongation of vortex length, heightened wall shear stress, and increased slope of velocity profiles downstream of the stenosed region. Furthermore, bulky obstruction of viscoelastic arteries as opposed to elastic, resulted in a maximum 5 percent increase in velocity profile and a 29.6% decrease in radial displacement. The zenith of shear stress occurs concomitantly with the velocity's peak within the stenosed area. Viscoelastic arterial wall shear stress at the stenosis site escalates due to the rapid expansion of the stenosis. The viscoelastic wall, responding with a blend of viscous and elastic characteristics to applied stress, undergoes slight deformation in shape. Following stress reduction, the wall gradually reverts to its original form, thus alleviating some of the applied stress. In contrast, the elastic wall retains its altered shape due to stress preservation within the material. Additionally, we ascertain an augmentation in radial displacement corresponding with increased artery stenosis.