The salient hemodynamic flow features in a stenosed artery depend not only on the degree of stenosis, but also on its location in the circulatory system and the physiological condition of the body. The nature of pulsatile flow waveform and local Womersley number vary in different regions of the arterial system and at different physiological state, which affects the local hemodynamic wall parameters, for example, the wall shear stress (WSS) and oscillatory shear index (OSI). Herein, we have numerically investigated the effects of different waveforms and Womersley numbers on the flow pattern and hemodynamic parameters in an axisymmetric stenosed arterial geometry with 50% diametral occlusion. Temporal evolution of the streamlines and hemodynamic parameters are investigated, and the time-averaged hemodynamic wall parameters are compared. Presence of the stenosis is found to increase the OSI of the flow even at the far-downstream side of the artery. At larger Womersley numbers, the instantaneous flow field in the stenosed region is found to have a stronger influence on the flow profiles of the previous time levels. The study delineates how an approximation in the assumption of inlet pulsatility profile may lead to significantly different prediction of hemodynamic wall parameters. 1. Introduction The investigation of the flow through a stenosed geometry is of interest because of its significance in connection to vascular diseases, like atherosclerosis which perpetrates to heart attack and stroke [1]. High level of cholesterol or triglycerides in blood results in continuous deposition of the fatty substances along the inner lining of the artery wall, constricting the flow passage and hardening the wall [2]. Numerous investigations have demonstrated that the altered shear stress activates mitogenic signaling pathways, promotes vascular cell proliferation and migration [3], enhances lipid deposition [4], and facilitates neointimal formation and atherogenesis [5]. Wootton and Ku [6] postulated a strong inverse correlation between wall shear stress and the atherosclerotic intimal thickening. Nerem [7] and Chiu et al. [8] concluded that the endothelial cells that line the arteries exhibit high cell division rates and low cell density near the reattachment point downstream to the stenosis, where the wall shear stress is low but the wall shear stress gradient (WSSG) is high. On the other hand, the increased pressure losses associated with flow separation at the stenosis reduce the flow rate, which can produce ischemia (localized absence of oxygen), needing surgical
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