An integrated fluid-chemical model toward modeling the thrombus formation in an idealized model of aortic dissection.

Abstract

Type B aortic dissection is a major aortic catastrophe that can be acutely complicated by rapid expansion, rupture, and malperfusion syndromes. The separation of the intima from aortic walls will form a second blood-filled lumen defined as "false lumen (FL)", where the thrombus is more likely to form due to the local stasis hemodynamic conditions. Complete thrombosis of FL is associated with a beneficial outcome while patency and partial thrombosis will lead to later complications. However, the thrombosis mechanism is still unclear and little is known about the impact of chemical species transported by blood flow on this process. The proteins involved in the coagulation cascade (CC) may play an important role in the process of thrombosis, especially in the activation and stabilization of platelets. Based on this hypothesis, a reduced-order fluid-chemical model was established to simulate CC in an aortic dissection phantom with two tears. A high level of fibrin is continuously observed at the top of the FL and some time-varying areas between two tears, indicating a high likelihood of thrombus formation there. This finding is consistent with the clinical observation. The time evolution of coagulation factors is greatly affected by local hemodynamics, especially in the high disturbance zone where the evolution has characteristics of periodic changes consistent with the flow field. The ability of the proposed model to reproduce the CC response provides a potential application to integrate with a model that can simulate platelet activities, forming a biochemical-based model which would help unveil the mechanisms of thrombosis in FL and the clinical decision of appropriate treatment.