Mathematical modeling of thrombosis hydrodynamic activation in stenosed vessels
Moscow Institute of Physics and Technology, Russian Federation, 141700, Dolgoprudny, Institutskiy per. 9, +7 (985) 983-61-19, email@example.com
1National Medical Research Center for Hematology, Health Ministry of Russian Federation, Russian Federation, 125167, Moscow, Novyy Zykovskiy proezd, 4
Platelet activation in intensive shear blood flows is possible through interaction with a molecule von Willebrand Factor (vWF). The initiation of this mechanism occurs only when overcritical shear stresses are reached. Such hydrodynamic conditions are observed both in norm and in pathology. Activated platelets can cause thrombotic complications such as heart attacks, strokes, or disrupt work of implantable devices.
Molecule vWF plays a key role in dynamic effect transfer of shear stress to the intracellular pathways of platelet activation. vWF consists of monomers, which have an A1 binding site with platelets GPIb receptors. Molecule vWF is present in the blood in the form of a globule, exposing insufficient number of A1 domains for platelets activation. Shear stress increase converts vWF to a more stretched form, in which more A1 domains become available for binding with platelets. When the shear stress exceeds a certain critical value, the unwound molecule vWF becomes capable of activating platelets. In a recent paper , it was shown how the shear stress and the length of vWF affect platelets activation.
In current work a spatially-distributed model of hydrodynamic activation of platelets is created. It allows to investigate hydrodynamic activation of platelets for various vessel geometries, flow conditions or vWF size distribution. The model can be used to evaluate risks of thrombotic complications in realistic vessels obtained by methods of diagnostic radiology.
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