PB1336 - Hemodynamic Flow Fields of Platelet-dependent Thrombus Formation in a Modified Folts Model

Background: Platelet aggregation in a carotid artery with atherosclerosis can lead to stroke. The stenosed geometry can trigger a shear and platelet-dependent thrombosis. The Folts-Model is a valuable in-vivo tool, developed to model this process and to test compounds that augment or inhibit thrombosis in stenosed arteries. Despite the significance use of this model, the hemodynamics, shear environment, and how it relates to the thrombus composition in this model remains less defined.

Aims: Quantify the flow field in the mouse carotid in the modified Folts-Model and correlate thrombus behavior with specific hemodynamics that can lead to vessel occlusion in this model.

Methods: Using the modified Folts-Model, carotid blood flow was measured using a Doppler flow probe. Thrombus growth over time was quantified and related to the local shear stress and flow through the vessel. Growth was quantified through kymographs of vessel diameter vs time. Thrombus geometry was extracted and matched to flow measurements. Through image processing, we recreated thrombus geometry in a computational fluid dynamics model created in ANSYS Fluent, while using the flow measurements for boundary conditions to quantify local shear conditions.

Results: Initial wall shear rates in the carotid are 500 1/s. Wall shear rates on the growing thrombus reaches 2250 1/s as the thrombus grows toward occlusion. It reaches a steady size of near roughly 70%, but shear rates remain spatially and temporally transient due to the pulsatility of flow with periodic collapse of the vessel onto the thrombus. This reduction in flow due to thrombus growth limits shear rates, despite the decreasing lumen. Histology was performed to validate the platelet-rich microstructure of the clots.

Conclusion(s): We were able to link different stages of dynamic shear changes that occur throughout thrmbus growth. These pulsatile, ever-changing flow environments provide us with an evidence-based way to link the model to carotid thrombi in humans.