Effect of stenotic shapes and arterial wall elasticity on the hemodynamics

The present study employs an arbitrary Lagrangian–Eulerian fluid–structure interaction approach to investigate pulsatile blood flow through a deformable stenosed channel. The flow is modeled by solving the incompressible continuity and momentum equations using finite element-based commercial solver COMSOL Multiphysics®. In this work, we explore the effects of different stenotic shapes—elliptical, round, and sinusoidal, degrees of stenosis (30%, 50%, and 70%), and arterial wall stiffnesses—0.5, 1.5, and 2.5 MPa on the velocity profile, pressure and wall shear stress distribution, and wall deformation. The oscillatory shear index (OSI) is analyzed to predict further plaque formation in the stenosed artery. We find that the flow velocity, wall shear stress, and pressure difference across the stenosed region increase with an increase in the stenotic severity and artery stiffness. The velocity profiles intersect at a radial location in the stenotic region termed critical radius, where relative magnitudes get reversed. With the increase in stenotic severity, the wall displacement decreases at the throat and increases at the upstream side. With the increase in wall stiffness, the wall deformation decreases, and shear stress increases, thereby increasing the pressure drop across the stenosed region. At a lower mass flow rate and a higher degree of stenosis, the vortices are formed upstream and downstream of the stenosed region for all stenotic shapes. The vorticity magnitude is found to be more than 21% higher for sinusoidal stenotic shape than round and elliptical ones. The effect of stenotic profile on the pressure drop characteristics shows that blood experiences maximum wall shear stress for the sinusoidal stenotic geometry, whereas the pressure drop is the maximum for the elliptical stenotic shape. The elliptical stenotic shape is more prone to further plaque formation than round and sinusoidal stenotic shapes. At lower Womersley number (Wo=2.76) corresponding to 60 beats per min heart beat rate, secondary vortices are formed downstream of the channel, causing higher OSI.