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Computational fluid dynamic modeling to predict wall shear stress in the cephalic vein of human subjects (588.1)
Author(s) -
Hammes Mary,
Boghosian Michael,
Kevin Cassel,
Hines Jane
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.588.1
Subject(s) - cephalic vein , medicine , shear stress , stenosis , blood flow , computational fluid dynamics , hemodialysis , fistula , vein , arch , cardiology , surgery , materials science , structural engineering , mechanics , composite material , engineering , physics
Background Cephalic arch stenosis (CAS) leads to access failure in hemodialysis patients with brachiocephalic fistula. The objective of this study was to use computational fluid dynamic modeling (CFD) to predict wall shear stress (WSS) in fistula access to determine the effects of increased arterial flow in the cephalic arch. Methods A venogram, Doppler and whole blood viscosity were performed pre‐fistula and at 3 months. Geometric measurements of arch angle and vein diameter were made. CFD of the cephalic arch was created to predict wall shear stress throughout the vessel. Results Eleven subjects receiving hemodialysis were studied. The arch angle decreased with a mean average of 133° at baseline to 116° at three months (p = 0.002). The venous diameter increased from 0.26 cm to 0.44 cm (p = 0.002). The blood flow increased from 3.95 cm/sec to 47.14 cm/sec (p < 0.001). A comparison of the CFD streamline plots between baseline and three months showed angle reduction, coupled with high flows leading to flow separation in most cases at three months. Flow separation was associated with a change in flow direction and low WSS. Conclusion Fistula creation results in increased arterial pressure and flow in the native vein. The vein dilates over three months with an observed decrease in [LOCAL] WSS made worse by the acute angulation of the arch, both contributing to intimal hyperplasia and CAS.Grant Funding Source : Supported By: NIH‐NDK 1 RO1 DK090769