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The technique of large-eddy simulation (LES) has been applied to the study of pulsatile flow through a modeled arterial stenosis. A simple stenosis model has been used that consists of a one-sided 50 percent semicircular constriction in a planar channel. The inlet volume flux is varied sinusoidally in time in a manner similar to the laminar flow simulations of Tutty (1992). LES is used to compute flow at a peak Reynolds number of 2000 and a Strouhal number of 0.024. At this Reynolds number, the flow downstream of the stenosis transitions to turbulence and exhibits all the classic features of post-stenotic flow as described by Khalifa and Giddens (1981) and Lieber and Giddens (1990). These include the periodic shedding of shear layer vortices and transition to turbulence downstream of the stenosis. Computed frequency spectra indicate that the vortex shedding occurs at a distinct high frequency, and the potential implication of this for noninvasive diagnosis of arterial stenoses is discussed. A variety of statistics have been also extracted and a number of other physical features of the flow are described in order to demonstrate the usefulness of LES for the study of post-stenotic flows. Keywords: Turbulent Flows, Turbulence Modeling, Stenotic Flows, Cardiovascular Flows, Computational Fluid Dynamics, Hemodynamics, Bio-fluid Dynamics, Blood Flow

The hinge region of a mechanical bileaflet valve is implicated in blood damage and initiation of thrombus formation. Detailed fluid dynamic analysis in the complex geometry of the hinge region during the closing phase of the bileaflet valve is the focus of this study to understand the effect of fluid-induced stresses on the activation of platelets. A fixed-grid Cartesian mesh flow solver is used to simulate the blood flow through a two-dimensional geometry of the hinge region of a bileaflet mechanical valve. Use of local mesh refinement algorithm provides mesh adaptation based on the gradients of flow in the constricted geometry of the hinge. Leaflet motion is specified from the fluid-structure interaction analysis of the leaflet dynamics during the closing phase from a previous study, which focused on the fluid mechanics at the gap between the leaflet edges and the valve housing. A Lagrangian particle tracking method is used to model and track the platelets and to compute the magnitude of the shear stress on the platelets as they pass through the hinge region. Results show that there is a boundary layer separation in the gaps between the leaflet ear and the constricted hinge geometry. Separated shear layers roll up into vortical structures that lead to high residence times combined with exposure to high-shear stresses for particles in the hinge region. Particles are preferentially entrained into this recirculation zone, presenting the possibility of platelet activation, aggregation, and initiation of thrombi. [ABSTRACT FROM AUTHOR]

The fluid dynamics during valve closure resulting in high shear flows and large residence times of particles has been implicated in platelet activation and thrombus formation in mechanical heart valves. Our previous studies with bi-leaflet valves have shown that large shear stresses induced in the gap between the leaflet edge and the valve housing results in relatively high platelet activation levels whereas flow between the leaflets results in shed vortices not conducive to platelet damage. In this study we compare the result of closing dynamics of a tilting disc valve with that of a bi-leaflet valve. The two-dimensional fluid-structure interaction analysis of a tilting disc valve closure mechanics is performed with a fixed grid Cartesian mesh flow solver with local mesh refinement, and a Lagrangian particle dynamic analysis for computation of potential for platelet activation. Throughout the simulation the flow remains in the laminar regime and the flow through the gap width is marked by the development of a shear layer which separates from the leaflet downstream of the valve. Zones of re-circulation are observed in the gap between the leaflet edge and the valve housing on the major orifice region of the tilting disc valve and are seen to be migrating towards the minor orifice region. Jet flow is observed at the minor orifice region and a vortex is formed which sheds in the direction of fluid motion as observed in experiments using PIV measurements. The activation parameter computed for the tilting disc valve, at the time of closure was found to be 2.7 times greater than that of the bi-leaflet mechanical valve and was found to be in the vicinity of the minor orifice region mainly due to the migration of vortical structures from the major to the minor orifice region during the leaflet rebound of the closing phase.

The adhesion of leukocytes to substrates is an important biomedical problem and has drawn extensive research. In this study, employing both single and compound drop models, we investigate how hydrodynamics interacts with an adherent liquid drop in a shear flow. These liquid drop models have recently been used to describe the rheological behavior of leukocytes. Numerical simulation confirms that the drop becomes more elongated when either capillary number or initial contact angle increases. Our results show that there exists a thin region between the drop and the wall as the drop undergoes large stretching, which allows high pressure to build up and provides a lift force. In the literature, existing models regard the leukocyte as a rigid body to calculate the force and torque acting on the drop in order to characterize the binding between cell receptors and endothelial ligands. The present study indicates that such a rigid body model is inadequate and the force magnitude obtained from it is less than half of that obtained using the deformable drop models. Furthermore, because of its much higher viscosity, the cell nucleus introduces a hydrodynamic time scale orders of magnitude slower than the cytoplasm. Hence the single and compound drops experience different dynamics during stretching, but exhibit very comparable steady-state shapes. The present work offers a framework to facilitate the development of a comprehensive dynamic model for blood cells.