Abstract

BackgroundAn autogenous arteriovenous fistula is the optimal vascular access for hemodialysis. In the case of brachiocephalic fistula, cephalic arch stenosis commonly develops leading to access failure. We have hypothesized that a contribution to fistula failure is low wall shear stress resulting from post-fistula creation hemodynamic changes that occur in the cephalic arch.MethodsTwenty-two subjects with advanced renal failure had brachiocephalic fistulae placed. The following procedures were performed at mapping (pre-operative) and at fistula maturation (8–32 weeks post-operative): venogram, Doppler to measure venous blood flow velocity, and whole blood viscosity. Geometric and computational modeling was performed to determine wall shear stress and other geometric parameters. The relationship between hemodynamic parameters and clinical findings was examined using univariate analysis and linear regression.ResultsThe percent low wall shear stress was linearly related to the increase in blood flow velocity (p < 0.01). This relationship was more significant in non-diabetic patients (p < 0.01) than diabetic patients. The change in global measures of arch curvature and asymmetry also evolve with time to maturation (p < 0.05).ConclusionsThe curvature and hemodynamic changes during fistula maturation increase the percentage of low wall shear stress regions within the cephalic arch. Low wall shear stress may contribute to subsequent neointimal hyperplasia and resultant cephalic arch stenosis. If this hypothesis remains tenable with further studies, ways of protecting the arch through control of blood flow velocity may need to be developed.

Highlights

  • We have hypothesized that a contribution to fistula failure is low wall shear stress resulting from post-fistula creation hemodynamic changes that occur in the cephalic arch

  • The percent low wall shear stress was linearly related to the increase in blood flow velocity (p < 0.01)

  • Primary brachiocephalic fistulae (BCF) for hemodialysis frequently lose patency because stenosis occurs in the cephalic arch, a vein segment that connects the cephalic to the axillary vein [1, 2]

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Summary

Introduction

Primary brachiocephalic fistulae (BCF) for hemodialysis frequently lose patency because stenosis occurs in the cephalic arch, a vein segment that connects the cephalic to the axillary vein [1, 2]. We have considered the alternative hypothesis that high blood flows develop in the cephalic vein due to fistula creation and lead to local regions with abnormally low wall shear stress (WSS) in curved segments such as the cephalic arch. Low WSS is known to promote neointimal hyperplasia (NH) [5], which would narrow the vein lumen, potentially further disrupting flow dynamics, and lead to cephalic arch stenosis (CAS). In the case of brachiocephalic fistula, cephalic arch stenosis commonly develops leading to access failure. We have hypothesized that a contribution to fistula failure is low wall shear stress resulting from post-fistula creation hemodynamic changes that occur in the cephalic arch

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