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Research Papers

Incomplete Restoration of Homeostatic Shear Stress Within Arteriovenous Fistulae

[+] Author and Article Information
Patrick M. McGah

Research Assistant
Department of Mechanical Engineering,
University of Washington,
Stevens Way, Box 352600,
Seattle, WA 98195
e-mail: pmcgah@uw.edu

Daniel F. Leotta

Research Engineer
Applied Physics Laboratory,
Center for Industrial and Medical Ultrasound,
University of Washington,
Box 355640,
Seattle, WA 98195

Kirk W. Beach

Professor Emeritus

R. Eugene Zierler

Professor
Department of Surgery,
Division of Vascular Surgery,
University of Washington,
Box 356410,
Seattle, WA 98195

Alberto Aliseda

Associate Professor
University of Washington,
Department of Mechanical Engineering,
Stevens Way, Box 352600,
Seattle, WA 98195

1Corresponding author.

Contributed by the Bioengineering Division of ASME for publication in the Journal of Biomechanical Engineering. Manuscript received April 18, 2012; final manuscript received November 7, 2012; accepted manuscript posted December 8, 2012; published online December 27, 2012. Assoc. Editor: Fotis Sotiropoulos.

J Biomech Eng 135(1), 011005 (Dec 27, 2012) (9 pages) Paper No: BIO-12-1149; doi: 10.1115/1.4023133 History: Received April 18, 2012; Revised November 07, 2012; Accepted December 08, 2012

Abstract

Arteriovenous fistulae are surgically created to provide adequate access for dialysis patients suffering from end-stage renal disease. It has long been hypothesized that the rapid blood vessel remodeling occurring after fistula creation is, in part, a process to restore the mechanical stresses to some preferred level, i.e., mechanical homeostasis. We present computational hemodynamic simulations in four patient-specific models of mature arteriovenous fistulae reconstructed from 3D ultrasound scans. Our results suggest that these mature fistulae have remodeled to return to ‘‘normal’’ shear stresses away from the anastomoses: about 1.0 Pa in the outflow veins and about 2.5 Pa in the inflow arteries. Large parts of the anastomoses were found to be under very high shear stresses $>15$ Pa, over most of the cardiac cycle. These results suggest that the remodeling process works toward restoring mechanical homeostasis in the fistulae, but that the process is limited or incomplete, even in mature fistulae, as evidenced by the elevated shear at or near the anastomoses. Based on the long term clinical viability of these dialysis accesses, we hypothesize that the elevated nonhomeostatic shear stresses in some portions of the vessels were not detrimental to fistula patency.

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Figures

Fig. 1

Three-dimensional ultrasound reconstructions of the four fistulae with the lumen colored by time-averaged wall shear stress (Eq. (3)) in Pa. (a), (b), (c), and (d) Reconstructions from patients 1, 2, 3, and 4, respectively. The view in each subfigure is shown from the skin toward the fistula. The bar labeled 20 mm shows the relative size of each figure.

Fig. 2

Streamwise blood velocity versus time for two cardiac cycles. The time history is taken from a point in the venous outflow of patient 1 about 5 mm downstream of the anastomosis in the center of the vessel. (a) The raw time-signal. (b) The time signal with the 5 cycle phase-averaged velocity removed. The inset shows the phase of the arterial inflow.

Fig. 3

Visualization of transitional flow vortices using the Q-criterion for patient no. 1 at (a) peak systole, and (b) end diastole. The value of Q is 0.5 when normalized by the mean centerline velocity and radius of the proximal artery.

Fig. 4

Shear stress duty factor DF distribution on the lumen for patient no. 1 using a threshold shear of 15 Pa. The bar labeled 20 mm shows the relative size. The large values of the duty factor in the proximal artery are due to the vessel curvature which produces a strong secondary helical flow. The large value of the duty factor on the anastomosis is due to the impingement and stagnation point flow.

Fig. 5

Space- and time-averaged shear (Eq. (3)) in Pa at 5 mm increments along the length of the proximal vein of all four patients. The data point of shear for patient no. 4 located at a distance of 2.5 mm is not shown on the scale but is equal to 12.9 Pa.

Fig. 6

Normalized highly stressed area Aτ/DA2 when τo=15 Pa in all four patients versus the mean centerline arterial inflow velocity squared U2. The solid line is a least squares regression. The coefficient of determination is 0.96 and p < 0.05.

Fig. 7

Space- and- time-averaged shear (Eq. (3)) in Pa at 5 mm increments along the proximal artery and proximal vein of patient 3. The symbols represent the simulated values in the artery (Sim. Art.) and vein (Sim. Vein), while the solid lines are the shear predicted by Poiseuille's law for the artery (Pois. Art.) and vein (Pois. Vein) with the same flow rate and average diameter.

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