Numerical simulations of the complex flows of complex (viscoelastic) fluids are investigated. The primary fluid investigated in this thesis is human blood, a complex fluid which can be modelled via viscoelastic constitutive models. The most commonly used constitutive models for viscoelastic fluids include the OldroydB, Giesekus, Johnson-Segalman, Finitely Extensible Non-Linear Elastic (FENE), Phan-Thein-Tanner (PTT) models etc. Our Numerical approach is based on the finite volume methods implemented on the OpenFOAM platform. We employ the Giesekus, Oldroyd-B, and Generalized Oldroyd-B viscoelastic constitutive models in this thesis, depending on the underlying context. Numerical validation of our results is conducted via the most used benchmark flow problems for viscoelastic fluid flow. The robust and efficient numerical methodologies are then deployed to investigate the flow characteristics, and hence illustrate various novel behavior, for blood flow in stenosed and bifurcated arteries. The present work took advantage of the availability of a reasonable set of viscoelastic constitutive model solvers within OpenFOAM, specifically the viscoelasticFluidFoam solver which we modified and developed to suit our focused needs for blood flow computations. The modified computational algorithms were successfully validated against well-known benchmark flow problems in the literature. Noting that the Giesekus viscoelastic constitutive model is a generalization of both the Oldroyd-B and Generalized Oldroyd-B models, the validation of results is carried out via the Giesekus model enabling us to develop a general-purpose code capable of simulating several viscoelastic constitutive models. The main results were otherwise presented for the Oldroyd-B and Generalized Oldroyd-B models as these are the most applicable to blood flow modelling. The results demonstrate that the velocity spurt through the stenosis is directly proportional to the constriction caused by the stenosis. The higher the blockage from the constriction, the higher the corresponding velocity spurt through the constriction. This velocity behavior, as the constriction blockage increases, correspondingly increase the wall shear stresses. High wall shear stresses significantly increase the possibility of rupture of the stenosis/blockage. This can lead to catastrophic consequences in the usual case where the stenosis is caused by tumor growth.