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Updated: Jul 15, 2025

In Vitro Model of Physiological and Pathological Blood Flow with Application to Investigations of Vascular Cell Remodeling
Published on: November 3, 2015
Hemodynamics in AVF over time: A protective role of vascular remodeling toward flow stabilization
Luca Soliveri1, Michela Bozzetto1, Paolo Brambilla2,3
1Department of Biomedical Engineering, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Bergamo, Italy.
Abstract:
The mechanisms underlying vascular stenosis formation in the arteriovenous fistula (AVF) for hemodialysis (HD) remain mostly unknown. Several computational fluid dynamics (CFD) studies have suggested a potential role for unsteady flow in inducing intimal hyperplasia and AVF stenosis, but the majority of these observations have been limited to a single time point after surgical creation. The aim of the present study was to investigate the relation between hemodynamic conditions and AVF vascular remodeling through a CFD longitudinal study. Non contrast-enhanced MR images and Doppler Ultrasound (US) examinations were acquired at 3 days, 40 days, 6 months, 1 year, and 1.5 years after surgery in a 72-year male referred for native radio-cephalic AVF. Three-dimensional AVF models were generated and high fidelity CFD simulations were performed using pimpleFoam, setting patient-specific boundary conditions derived from US. Morphological and hemodynamic changes over time were then analyzed. Analysis of vessel morphology and hemodynamics during follow-up showed that the AVF had a successful maturation process, characterized by a massive arterial and venous dilatation within the 6 months after surgery, a corresponding increase in blood flow volume and important flow instabilities. Between 6 months and 1 year, a stenosis developed in the juxta-anastomotic vein and caused AVF failure at 1.5 years. The development of stenosis was paralleled by the regularization of blood flow velocity pattern and consequent decrease in the near-wall disturbed flow metrics. These results suggest that development of intimal hyperplasia and vessel stenosis, triggered by unsteady flow, could be the result of vascular inward remodeling toward regularization of turbulent-like flow.
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