Refining a numerical model for device-induced thrombosis and investigating the effects of non-Newtonian blood models.

Thrombosis is one of the main causes of failure in device implantation. Computational thrombosis simulation is a convenient approach to evaluate the risk of thrombosis for a device. However, thrombosis is a complicated process involving multiple species and reactions. Application of a macroscopic, single-scale computational model for device-induced thrombosis is a cost-effective approach. The current study has refined an existing thrombosis model, which simulated thrombosis by tracing four species in blood: non-activated platelets, activated platelets, surface adherent platelets, and ADP. Platelets are activated mechanically by shear stress, and chemically by ADP. Platelet adhesion occurs on surfaces with low wall shear stress with platelet aggregation inhibited in regions of high shear stress. The study improves the existing thrombosis model by: 1) Modifying the chemical platelet activation function so that ADP activates platelets; 2) Modifying the function describing thrombus deposition and growth to distinguish between thrombus deposition on wall surfaces and thrombus growth on existing thrombus surfaces; 3) Modifying the thrombus breakdown function to allow for thrombus breakdown by shear stress; 4) Modeling blood flow as non-Newtonian. The results show that the inclusion of ADP and the use of a non-Newtonian model improve agreement with experimental data.