Loading...

Numerical Simulation of Blood clot Formation and Growth and Investigating the Effect of Blood Rheology on this Process

Tork, Ahmad Reza | 2025

0 Viewed
  1. Type of Document: M.Sc. Thesis
  2. Language: Farsi
  3. Document No: 57830 (08)
  4. University: Sharif University of Technology
  5. Department: Mechanical Engineering
  6. Advisor(s): Firoozabadi, Bahar
  7. Abstract:
  8. Blood clot formation in the heart vessels begins with damage to the vessel wall. This triggers the deposition of platelets at the site of injury. Finally, to stabilize the clot, a fibrin network forms over the accumulated platelets. In this study, a mathematical model was employed to analyze the growth of blood clots in stenosed vessels. The blood hydrodynamics were modeled by solving the continuity and Navier-Stokes equations, while the transport species involved in biological reactions were captured using the convection-diffusion-reaction equations. The simulations were conducted using Fluent software in two modes: fixed geometry and moving geometry. In the fixed geometry case, platelet deposition is assumed to have no impact on blood flow. The simulation results indicate that blood rheology significantly influences the flow pattern and platelet deposition, particularly in the post-maximal stenosis regions. In these areas, the presence of recirculation zones and consequently low shear rates makes the effects of blood rheology more pronounced. Among the non-Newtonian models examined, the Cross model produced results closest to the Newtonian assumption for blood, whereas the Casson model showed the greatest difference. This is because, in the mathematical formulation of non-Newtonian viscosity models based on shear rate, the Cross model exhibits behavior most similar to experimental results, within the shear rate range studied in this work (<10 s⁻¹). In contrast, the Casson model shows the greatest deviation in viscosity behavior compared to the other models. For the case of 35% stenosis and a Reynolds number of 120, the Casson model reduced platelet deposition in the recirculation zones by approximately 70% compared to the Newtonian assumption. Additionally, the simulation results revealed that as the Reynolds number and stenosis degree increased, the difference between the Newtonian assumption and non-Newtonian models became smaller. The study on the effect of heparin on platelet deposition revealed that an increase in heparin concentration led to a reduction in platelet deposition, particularly in the regions of maximal stenosis, aligning with clinical observations. Additionally, the results indicate that regardless of the size and location of injury, platelet activator agonists are primarily accumulated in the post-maximal stenosis regions. However, reducing the length of the injured area led to a decrease in the concentration of these species. Specifically, adenosine diphosphate concentration decreased by approximately 40%, while thromboxane levels dropped by nearly an order of magnitude. This significant reduction in thromboxane concentration is attributed to its strong dependence on injury size, as defined by the mathematical formulation. In the dynamic geometry mode, blood clot growth influenced blood flow based on the number of deposited platelets. This mode also allowed for the investigation of heparin's effect on occlusion time. The simulation results showed that increasing heparin concentration from zero to 4.5 units/mL extended the occlusion time from approximately 120 seconds to over 330 seconds, highlighting the significant role of heparin in regulating occlusion dynamics
  9. Keywords:
  10. Blood Clot ; Thrombosis Formation ; Platelet Agregation ; Vascular Occlusion ; Non-Newtonian Models ; Heparin ; Occlusion Time ; Stenosed Vessels ; Platelet Deposition

 Digital Object List

 Bookmark

No TOC