The study of hemodynamics is particularly important in medicine and biomedical engineering as it is crucial for the design of new implantable devices and for understanding the mechanism of various diseases related to blood flow. In this study, we experimentally identify the cell free layer (CFL) width, which is the result of the Fahraeus–Lindqvist effect, as well as the axial velocity distribution of blood flow in microvessels. The CFL extent was determined using microscopic photography, while the blood velocity was measured by micro-particle image velocimetry (μ-PIV). Based on the experimental results, we formulated a correlation for the prediction of the CFL width in small caliber (D < 300 μm) vessels as a function of a modified Reynolds number (Re∞) and the hematocrit (Hct). This correlation along with the lateral distribution of blood viscosity were used as input to a “two-regions” computational model. The reliability of the code was checked by comparing the experimentally obtained axial velocity profiles with those calculated by the computational fluid dynamics (CFD) simulations. We propose a methodology for calculating the friction loses during blood flow in μ-vessels, where the Fahraeus–Lindqvist effect plays a prominent role, and show that the pressure drop may be overestimated by 80% to 150% if the CFL is neglected.

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The Abdominal Aortic Aneurysm (AAA) is a local dilation of the abdominal aorta and it is a cause for serious concern because of the high mortality associated with its rupture. Consequently, the understanding of the phenomena related to the creation and the progression of an AAA is of crucial importance. In this work, the complicated interaction between the blood flow and the AAA wall is numerically examined using a fully coupled Fluid-Structure Interaction (FSI) method. The study investigates the possible link between the dynamic behavior of an AAA and the blood viscosity variations attributed to the haematocrit value, while it also incorporates the pulsatile blood flow, the non-Newtonian behavior of blood and the hyperelasticity of the arterial wall. It was found that blood viscosity has no significant effect on von Mises stress magnitude and distribution, whereas there is a close relation between the haematocrit value and the Wall Shear Stress (WSS) magnitude in AAAs. This WSS variation can possibly alter the mechanical properties of the arterial wall and increase its growth rate or even its rupture possibility. The relationship between haematocrit and dynamic behavior of an AAA can be helpful in designing a patient specific treatment.

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