Research Article Simulations of Magnetohemodynamics in Stenosed Arteries in Diabetic or Anemic Models Aiman Alshare 1 and Bourhan Tashtoush 2 1 Mechanical Engineering Department, German Jordanian University, Amman 11180, Jordan 2 Mechanical Engineering Department, Jordan University of Science and Technology, Irbid 22110, Jordan Correspondence should be addressed to Aiman Alshare; aiman.share@gju.edu.jo Received 5 November 2015; Revised 11 January 2016; Accepted 19 January 2016 Academic Editor: Guan H. Yeoh Copyright © 2016 A. Alshare and B. Tashtoush. Tis is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Pulsatile fow simulations of non-Newtonian blood fow in an axisymmetric multistenosed artery, subjected to a static magnetic feld, are performed using FLUENT. Te infuence of artery size and magnetic feld intensity on transient wall shear stress, mean shear stress, and pressure drop is investigated. Tree diferent types of blood, namely, healthy, diabetic, and anemic are considered. It is found that using Newtonian viscosity model of blood in contrast to Carreau model underestimates the pressure drop and wall shear stress by nearly 34% and 40%, respectively. In addition, it is found that using a magnetic feld increases the pressure drop by 15%. Generally, doubling the artery diameter reduces the wall shear stress approximately by 1.6 times. Also increasing the stenosis level from moderate to severe results in reduction of the shear stress by 1.6 times. Furthermore, doubling the diameter of moderately stenosed artery results in nearly 3-fold decrease in pressure drop. It is also found that diabetic blood results in higher shear stress and greater pressure drop in comparison to healthy blood, whereas anemic blood has a decreasing efect on both wall shear stress and pressure drop in comparison to healthy blood. 1. Introduction Atherosclerosis is an accumulation of cholesterol-laden plaque in arterial walls that causes a narrowing or stenosis and a loss of elasticity in the arteries at various sites. Te diseased arteries ofen result in heart attacks and strokes both of which are leaders in human mortality. Te major cause of stroke is blood vessel blockage or plaque rupture. Narrowing of an arterial lumen tends to occur in regions of disturbed fow and oscillating wall shear stress (WSS). Tan et al. [1] linked the growth, progression, and structure of plaque in a 70% carotid symmetric stenosis at rupture to the oscillating wall shear stresses using pulsatile transitional simulations. Considering axially asymmetric stenosis and Newtonian fuid model Gao et al. [2] found that the Womersley number has a great infuence on the vortex generation and the WSS distribution and to a lesser extent on the Reynolds number. Grinberg et al. [3] analyzed the fow in stenosed carotid artery using three-dimensional transient model and a simplifed two-dimensional slice, since the latter is more appropriate as clinical tool. Teir results revealed that regions of unsteady laminar fow characterize the state of the fow and a subregion of turbulence, starting downstream of the stenosis and extending about fve to six centimeters farther downstream. Te fow in the subregion is found to laminarize as the Reynolds number is decreased. Pulsatile fow of Newtonian blood through stenosed porous medium with periodic body acceleration under the infuence of a uniform transverse magnetic feld was studied by Das and Saha [4]. Te study proposed that varying the efect of the magnetic feld in, for example, clinical magnetotherapy, can regulate the volumetric fow rate. Numerical simulations have been proposed by Ku et al. [5] as a method for predicting changes in fow distributions and patterns from surgical bypass procedure. Te simula- tions’ results were temporally and spatially averaged and compared against measurements obtained using magnetic resonance imaging (MRI) techniques for a phantom model Hindawi Publishing Corporation Computational and Mathematical Methods in Medicine Volume 2016, Article ID 8123930, 13 pages http://dx.doi.org/10.1155/2016/8123930