Abstract 3143: Computational Modeling Of Non-homeostatic Changes Within An Arterial-venous Fistula System Using In Vivo Validation To Understand Mechanical Causes Of Fistula Failure

Abstract

Introduction: Arteriovenous fistula (AVF) failure is a clinical problem for end stage renal patients seeking durable long term dialysis access. AVF failure is not fully understood, but linked to neointimal hyperplasia (NH). Understanding the hemodynamic factors that may trigger NH response is important for minimizing this clinical problem. Methods: A validated murine AVF model defined the geometry and boundary conditions for the computational model. Anesthetized mice underwent laparotomy and aorta-IVC puncture. Ultrasound specified blood flow velocity within the vessels. In vivo CT angiography scans were segmented using 3D software (Simpleware ScanIP) to establish global geometry which was imported into Xflow, a fluid dynamics simulation software. Velocity, static pressure, and turbulence were averaged along the length of the vein above and below the fistula in this model, a stenotic vein model, and a stenotic fistula model. Results: Velocity and turbulence significantly increases in the peri-fistula vein and dramatically increases in systole phase. Velocity, turbulence, and static pressure peak in the stenotic vein. When the fistula is stenosed, native flow is restored. Conclusions: The presence of AVF dramatically changes the hemodynamics of the native vein. Increased velocity and turbulence in the peri-fistula vein are significant and peak in systole. Venous stenosis substantially strains the system, demonstrated by the high static pressures proximal to the stenosis. The gradients of high turbulence directly correlate with in vivo histology measurements of neointimal hyperplasia thickness changes that have been previously reported. These results may be used to predict how the underlying hemodynamics within a fistula system preclude biological responses from the tissue. We conclude that non-homeostatic hemodynamics, namely increased venous velocity, turbulence, and static pressure may be a potential trigger for NH and ultimately fistula failure.