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Lipid core plaques are the major cause of the vascular stenosis and heart attacks. Accumulation of Low-Density Lipoproteins (LDLs) across the atherosclerotic lesions, leads to the hardening of the arterial wall and causes cross sectional narrowing of the artery. Among different arterial wall models, Multilayer model gives accurate LDL concentration across the layers. In this study LDL accumulation in the four-layer carotid artery is investigated numerically. Navier-Stokes equations along with Darcy’s model for the porous regions and the convection-diffusion mass transport equation are employed. Blood considered as a Newtonian fluid and the artery’s wall is assumed to be a porous rigid medium. Due to the negligible pulsatile effect of the flow on the LDL concentration, equations are solved in the steady state condition. In this paper LDL concentration across the layers is considered under normal blood pressure to examine effects of the LDL’s size and the hypertension on the LDL accumulation. Furthermore, a comparison between normal endothelium and the leaky junction is performed. Results indicate that the normal endothelium plays a crucial role in prevention LDL accumulation in the arterial wall.

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Lipid solutes in blood such as Low-Density Lipoproteins (LDLs) are the major cause of most cardiovascular diseases. Increase of fatty materials in the blood flow endanger personal healthiness and enhance possibility of cardio and cerebrovascular infarctions. In order to provide nutritional blood for different tissues, heart sends pulsatile flow with high pressure to the circulatory system such that LDL particles spread over the entire body. Contraction and expansion of the heart create pulsatile flow that affect blood hemodynamics and LDL mass transfer in vessels. In this paper, effects of the pulsatile flow on LDL mass transport in a multilayered artery with atherosclerotic plaques are investigated numerically. In order to apply pulsatile flow in the artery, a set of specific-person flow and pressure pulses, which are resulted from the ultrasound method, are employed directly. Results indicate that pulsatile flow increases LDL concentration both on the luminal surface and across arterial layers and produces interesting periodic concentration patterns in these regions. Moreover, pulsatile effect intensifies remarkable reversal flow right at post-stenotic regions of plaques locations, where the flow is recirculated naturally, and lowers LDL accumulation.