Abstract: This dissertation encompasses both a CFD analysis of flow in normal and diseased carotid arteries as well as a numerical study of the flow of high hematocrit blood. In our CFD studies, pulsatile blood flow is simulated in a three dimensional carotid bifurcation using fully coupled fluid-structure numerical methods. Using this computational model, we assess the variation among different wall models. Specifically, how does the effect of disease progression on the material properties of the wall influence calculations of blood flow in the carotid bifurcation and how computationally intensive does an arterial wall description need to be in order to be dependable? Increasing levels of disease are incorporated as stiffer walls by increasing the corresponding Young's modulus. An increasing order of refinement of arterial wall description is: rigid, isotropic, and orthotropic walls respectively. Qualitative and statistical differences between flows relevant to atherosclerotic risk factors were calculated and analyzed. The results show more complex flow dynamics, less atherogenic levels of wall shear stress, and lower wall shear stress temporal gradients in models with healthier wall properties, features which are also found for the flows in vessels with diseased orthotropic wall properties. In the second study we explore the effects of increased hematocrit due to blood doping in athletes and their clinical consequences. The Navier-Stokes equation is exploited to derive velocity in the coronary artery as a non-linear function of viscosity. We show that increasing hematocrit dramatically decreases and flattens the velocity profile. This combination of slower flow with a greater area of low shear rate illustrates the increased risk of thrombus formation with increased hematocrit.