Abstract-Alterations in mass transport patterns of lowdensity lipoproteins (LDL) and oxygen are known to cause atherosclerosis in larger arteries. We hypothesise that the species transport processes in coronary arteries may be affected by their physiological motion, a factor which has not been considered widely in mass transfer studies. Hence, we numerically simulated the mass transport of LDL and oxygen in an idealized moving coronary artery model under both steady and pulsatile flow conditions. A physiological inlet velocity and a sinusoidal curvature waveform were specified as velocity and wall motion boundary conditions. The results predicted elevation of LDL flux, impaired oxygen flux and low wall shear stress (WSS) along the inner wall of curvature, a predilection site for atherosclerosis. The wall motion induced changes in the velocity and WSS patterns were only secondary to the pulsatile flow effects. The temporal variations in flow and WSS due to the flow pulsation and wall motion did not affect temporal changes in the species wall flux. However, the wall motion did alter the time-averaged oxygen and LDL flux in the order of 26% and 12% respectively. Taken together, these results suggest that the wall motion may play an important role in coronary arterial transport processes and emphasise the need for further investigation.
Hemodialysis treatment requires a patient's blood circulation to be connected to artificial kidney extracorporeal (EC) circulation through a vascular access. In chronic patients, the vascular access is normally created by an artero-venous (AVF) fistula, where part of the peripheral arterial blood flows along a venous vessel. The connection is made by inserting two needles into the venous vessel. Blood is drawn to the EC along the arterial needle and is returned to the patient along the venous needle. In this study, we simulated the hemodynamics of vascular access with particular focus on the region downstream to the venous needle in order to analyze the influence of return flow (Qb) on blood circulation. A three dimensional CFD model of vascular access circulation was developed and various blood flow conditions were simulated. Simulation results predicted a critical circulation downstream to the needle tip due to the confluence between the return flow and the access flow. A vortex recirculation was evident in this region. Vortex extension appeared only for Qb values higher than 40% of the access flow and was limited to a zone few centimetres from the needle tip in the downstream direction. CFD simulations allowed a detailed study of the complex hemodynamics in the vascular access region surrounding the inserted needle which would otherwise be difficult to measure experimentally.
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