Haemodynamic and clot modelling in venous valves with variable aperture

George, Sunday

Haemodynamic and clot modelling in venous valves with variable aperture

Thesis / Dissertation

2026

Publisher

University of Cape Town

Department

Department of Mechanical Engineering

Faculty

Faculty of Engineering and the Built Environment

Abstract

The occurrence of deep vein thrombosis (DVT) has been linked to dysfunctional venous valves, leading to diseases like chronic venous insufficiency (CVI), varicose veins, and pulmonary embolism (PE). The thrombus initiates within the valve pockets, primarily driven by disturbed haemodynamic, prolonged residence time, and biochemical interactions that trigger the coagulation cascade. Understanding the complex interplay between flow conditions, valve geometry, and coagulation kinetics is crucial for improving DVT risk assessment and treatment strategies. While in vivo and in vitro studies provide valuable insights, they often have limited spatial and temporal resolution, making computational fluid dynamics (CFD) an important tool for elucidating clot formation in venous environments. Five idealized, two-dimensional, symmetric valve geometries were modelled, namely 50%, 70%, 70- 70%, 50-50%, and 70-50% valve openings, with smaller apertures (e.g., 50%) representing pathological cases associated with venous disease. The valve was assumed to remain static at its equilibrium opening phase rather than undergoing dynamic motion. The simulations, conducted in ANSYS Fluent Academic, modelled steady and pulsatile flow conditions with a Newtonian fluid assumption. A reduced coagulation cascade was adopted to track thrombin-fibrinogen interactions. A convection-diffusion reaction framework was implemented to model the transport and reaction of biochemical species, and thrombin was introduced as a scalar at the sinus wall. The Michaelis-Menten equation was incorporated to describe enzyme-mediated fibrin formation. A qualitative comparison of how valve apertures contribute to clot growth size and a quantitative comparison of reactive and non-reactive thrombin concentrations were made. Maximum fibrin deposition was analysed using two measurement approaches: random cell-based measurements, which captured localized peak fibrin accumulation at each time step, and probe point measurements, which provided insights into temporal fibrin distribution at the deepest region of the valve pocket. The results revealed that pulsatile flow led to larger and more rapidly forming clots than steady flow conditions. Smaller valve openings exhibited greater thrombin accumulation and extensive clot formation, while larger openings facilitated thrombin clearance, reducing thrombosis risk. The distal valve pockets consistently displayed higher thrombin and fibrin concentrations in the double-valve configurations, becoming fully occluded with clot. The study highlights the importance of valve geometry and haemodynamic forces in thrombus formation, providing critical insights for DVT initiation and propagation. To further refine the understanding of venous thrombogenesis, future research should incorporate three-dimensional modelling and patient-specific geometries.