Numerical and Magnetic Resonance Imaging Studies for Device-Induced Thrombosis
Open Access
- Author:
- Yang, Ling
- Graduate Program:
- Bioengineering
- Degree:
- Doctor of Philosophy
- Document Type:
- Dissertation
- Date of Defense:
- June 18, 2020
- Committee Members:
- Keefe B Manning, Dissertation Advisor/Co-Advisor
Keefe B Manning, Committee Chair/Co-Chair
Francesco Costanzo, Committee Member
Thomas Neuberger, Committee Member
Xiaofeng Liu, Outside Member
Christopher Alan Siedlecki, Committee Member
Daniel J Hayes, Program Head/Chair - Keywords:
- thrombosis
medical device
computational fluid dynamics
magnetic resonance imaging - Abstract:
- Thrombosis is one of the main causes of failure for cardiovascular devices. Better device design requires better understanding of the mechanisms of thrombosis. To minimize the risk of thrombosis due to implantation of medical devices, it is necessary to develop an accurate computational thrombosis model that can be used to evaluate the risk of thrombosis for cardiovascular devices and help better understand the relationship between hemodynamics and thrombosis. The current study achieves this goal by fulfilling the following specific aims: 1) Perform in vitro magnetic resonance imaging (MRI) experiments for quantification of thrombus deposition and growth within a sudden expansion geometry in real-time. And 2) develop and refine a computational model for device-induced thrombosis. The experimental method is detailed in Chapter 3, where thrombosis within a backward-facing step (BFS), or sudden expansion, was investigated using bovine and human blood circulated through the BFS model for 30 min. Real-time three-dimensional flow compensated MRI, supported with Magnevist, a contrast agent improving thrombus delineation, was applied to quantify thrombus deposition and growth within the model. The results are available in Chapter 5, which show that thrombus sizes increased during the first 15 min and stabilized after 20 min. The BFS model induced a flow recirculation region, which facilitated thrombosis. Blood properties, including viscosity, hematocrit, and platelet count affected thrombosis. In comparison to bovine blood, human blood resulted in smaller thrombus formation. The computational method is detailed in Chapter 4, where an existing thrombosis model was refined and applied to simulate thrombosis in a three-dimensional BFS model. Platelets were assumed to be activated mechanically by shear stress and chemically by adenosine diphosphate (ADP). Within the geometry, region with low shear stress promoted platelet aggregation and that with high shear stress promoted breakdown of the aggregate. Effects of pulsatile flow and non-Newtonian blood behavior were investigated. The simulation results were compared with available experimental data for model validation. The results are available in Chapter 5, which show that the chemical platelet activation by ADP dominated the thrombosis procedure after 5 minutes of blood flow. The pulsatile flow and non-Newtonian blood behavior suppressed thrombus deposition and growth within the BFS model, while the steady, Newtonian blood flow enhanced thrombosis. Overall, the current study provides more experimental data for device-induced thrombosis, fills the gap between numerical simulations and experimental work, and contributes to development of more accurate thrombosis models.