Direct numerical simulation of a pulsatile flow in a stenotic channel using immersed boundary method

A three‐dimensional direct numerical simulation model coupled with the immersed boundary method has been developed to simulate a pulsatile flow in a planar channel with single and double one‐sided semicircular constrictions. For relevance to blood flow in large arteries, simulations have been performed at Reynolds numbers of 750 and 1000. Flow physics and resultant wall shear stress (WSS)‐based hemodynamic parameters are presented. The instantaneous vortex dynamics, mean flow characteristics, and turbulent energy spectra are evaluated for flow physics. Subsequently, three WSS‐based parameters, namely the time‐averaged WSS, oscillatory shear index, and relative residence time, are calculated over the stenotic wall and correlated with flow physics to identify the regions prone to atherosclerotic plaque progression. Results show that the double stenotic channel leads to high‐intensity and broadband turbulent characteristics downstream, promoting critical values of the WSS‐based parameters in the post‐stenotic areas. In addition, the inter‐space area between two stenoses displays multiple strong recirculations, making this area highly prone to atherosclerosis progression. The effect of stenosis degree on the WSS‐based parameters is studied up to 60% degree. As the degree of occlusion is increased, larger regions are involved with the nonphysiological ranges of the WSS‐based parameters. A three‐dimensional direct numerical simulation model coupled with the immersed boundary method has been developed to simulate a pulsatile flow in a planar channel with single and double one‐sided semicircular constrictions. Flow physics in stenotic channels are elucidated with regard to vortex dynamics, mean flow characteristics, and turbulent energy spectra. Three hemodynamic wall parameters, namely the time‐averaged wall shear stress, oscillatory shear index, and relative residence time, are evaluated to identify the regions prone to atherosclerotic plaque progression.