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Session: Poster session 2 (Odd numbers)
Session starts: Friday 27 January, 10:00
Presentation starts: 10:00

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Mohammad Rezaeimoghaddam (Department of Biomedical Engineering, Eindhoven University of Technology, Postbus 513, Eindhoven 5600 MB, The Netherlands)
Bregje in 't Veld (Department of Biomedical Engineering, Eindhoven University of Technology, Postbus 513, Eindhoven 5600 MB, The Netherlands)
Lotte Piek (Department of Biomedical Engineering, Eindhoven University of Technology, Postbus 513, Eindhoven 5600 MB, The Netherlands)
Frans van de Vosse (Department of Biomedical Engineering, Eindhoven University of Technology, Postbus 513, Eindhoven 5600 MB, The Netherlands)

Abstract:
Autologous veins are widely used in bypass surgeries because of their availability, ease of use, and lower infection risk compared to synthetic grafts. However, the poor long-term outcomes of venous grafts (VGs) are mainly due to the luminal narrowing that results from neointimal hyperplasia (NIH) and subsequent superimposed thrombosis. Hence, the main challenge is detection of progressive vascular wall thickening due to NIH and avoid sudden thrombus formation. In spite of decades of experience in animal experiments, vascular tissue engineering design, and experimental trial-and-error, novel approaches are urgently required. Computational models are powerful tools that can provide great support and information in medical research. In this study two major processes responsible for VG failure, are analyzed using a computational model of thrombus formation in relation with NIH. In this study, a novel continuum model of platelet activation, aggregation, and essential regulators of the coagulation cascade is used to describe transport and reaction of biochemical agonists and predict thrombosis. The current model includes the features of our previous deposited bounded platelet model including shear induced platelet activation and embolization [1]. This model also contains von Willebrand factor (vWF) conformational change which stretched vWF can be bound to platelets integrins and collagen. The NIH model is based on the conservation of mass between VSMCs and the migration of cells between media and intima. The VSMCs phenotypical change from quiescent cells, migration from the media, proliferation and apoptosis are solved with a system of ordinary differential equations. A moving boundary technique is used to change computational nodes and alter the lumen diameter corresponds to NIH at each time step. The computational domain consists of a 2D channel with a semi-ellipse which represents stenosis at the bottom wall. This computational model will enable identifying key factors associated with the VG failure, resulting in new insights that are critical for guidelines to ensure patency of grafts. The results also accurately describe the interactions between the regulatory network of the coagulation cascade, agonist concentrations and dynamics of platelet deposition and fibrin due to hemodynamics. Ref: [1] M Rezaeimoghaddam and FN van de Vosse. J. Biomech. 2022.