Abstract
Computer simulations were performed to study the transport of red blood cells and platelets in high shear flows, mimicking earlier published in vitro experiments in microfluidic devices with high affinity for platelet aggregate formation. The goal is to understand and predict where thrombus formation starts. Additionally, the need of cell-based modelling in these microfluidic devices is demonstrated by comparing our results with macroscopic models, wherein blood is modelled as a continuous fluid. Hemocell, a cell-based blood flow simulation framework is used to investigate the transport physics in the microfluidic devices. The simulations show an enlarged cell-depleted layer at the site where a platelet aggregate forms in the experiments. In this enlarged cell-depleted layer, the probability to find a platelet is higher than in the rest of the microfluidic device. In addition, the shear rates are sufficiently high to allow for the von Willebrand factor to elongate in this region. We hypothesize that the enlarged cell-depleted layer combined with a sufficiently large platelet flux and sufficiently high shear rates result in an haemodynamic environment that is a preferred location for initial platelet aggregation.
Highlights
Arterial thrombosis occurs in vessels with a pathological shear rate caused by for example a stenosed vessel due to atherosclerosis [1] or by disturbed flow around medical device [2]
The suspended red blood cells (RBCs) and platelets are modelled by a discrete element method (DEM) and fluid–structure coupling is achieved via the immersed boundary method (IBM)
We studied the influence of RBC on haemodynamic parameters in microfluidic devices to better understand how the transport physics influence platelet aggregation
Summary
Arterial thrombosis occurs in vessels with a pathological shear rate (greater than 5000 s−1) caused by for example a stenosed vessel due to atherosclerosis [1] or by disturbed flow around medical device [2]. In comparison with venous thrombosis, the typical coagulation cascade is less important in arterial thrombosis. The reason for this is that the flow is faster in arteries and the coagulation cascade happens on a longer timescale (minutes) than the aggregation of platelets (seconds) in these fast flows. At high shear rates the vWF uncoils [4] This uncoiling can happen when the vWF is free flowing in the blood or when it is bound to a prothrombotic surface (collagen). The shear rate threshold for the uncoiling of free-flowing vWF is around 5000 s−1 [4] and for bounded vWF it is around 1000 s−1 [5]. The vWF slows the platelets down to facilitate the binding of a platelet to collagen or platelet–integrin binding to vWF, forming a stable platelet aggregate [7]
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