A computational model of chemically- and mechanically-induced thrombus formation in cerebral aneurysms

Thrombosis, the process of pathological blood clot formation, is a major consideration in the development of cardiovascular diseases and in the design of endovascular devices. Thrombosis is governed by both biochemical and mechanical considerations. Experimental evidence suggests that changes in blood shear rate, i.e., spatial shear gradients, play a critical role in thrombogenesis by controlling the process of platelet aggregation. In light of the above, understanding and predicting thrombus onset and growth in various physiological and pathological settings requires accounting for blood shear changes. The main goal of the current work is to create a comprehensive computational model of chemically- and mechanically-induced thrombus formation that accounts for the effects of shear gradients and extends our previous framework. Relative to our previous modeling, the current model was improved by including the non-Newtonian rheological blood behavior, fibrin fiber generation, and the local increase in fluid viscosity associated with thrombus formation. The model was applied to the specific case of cerebral aneurysms, and the results were consistent with experimental data of thrombus formation in two idealized aneurysm geometries, suggesting the model's ability to produce thrombus spatial and temporal profiles that are consistent with experimental observations. An important finding is that thrombus formation is driven by spatial shear gradients, while subsequent thrombus growth is governed by both mechanical and chemical factors. We believe that the current model constitutes a robust tool for the evaluation of thrombus evolution in scenarios of blood flow disturbance and for the optimization of the cardiovascular device design flow path.