Incomplete Restoration of Homeostatic Shear Stress Within Arteriovenous Fistulae

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.

Aortic pulse pressure homeostasis emerges from physiological adaptation of systemic arteries to local mechanical stresses

“…3) were first developed by Nguyen et al (46), who assumed that chronic adaptation is functionally similar to the acute shear stress-induced vasodilation and wall stress-induced vasoconstriction of muscular arteries (3,17,20,24,60) and microvessels (28,55,56,66). These adaptive rules were consistent with reported mechanisms of endothelial mechanotransduction (7) and observations from human clinical studies (9,37,39). Although most studies have focused on pathological changes in wall stiffness (34,47), simulations by Nguyen et al (46) supported the hypothesis that the elastic modulus must decrease with wall circumferential stress to yield physiological remodeling.…”

“…Consistent with in vivo experiments (9,39), our model predicted that adaptation to perturbations would not return the local mechanical stresses and pulse pressures back to baseline values (Figs. 4 and 5).…”

“…It is exceedingly difficult to control endothelial shear stress and wall circumferential stress in vivo. Adaptation-induced changes in radius, wall thickness, or stiffness affect mechanical stresses (9,17,37,39,75), even when luminal pressure and flow can be maintained (3,38,43,66). The inability to make mechanical stresses controlled, independent variables in vivo is an inescapable consequence of arterial growth and remodeling (22,55).…”

A predictive framework to elucidate venous stenosis: CFD & shape optimization

“…al. [79] ). Our model predicts an increase to 63%, which agrees acceptably with the patient-specific data.…”

Suppressing unsteady flow in arterio-venous fistulae

“…25 More recent work, undertaken specifically in the context of vascular fluid mechanics, includes studies of stenotic flows, 26 pulsatile flow in curved pipes, [27][28][29][30] flow in helical pipes, [31][32][33][34] and flow at junctions. [35][36][37] In terms of simulating flow in AVF configurations, there have been a range of previous Computational Fluid Dynamics (CFD) studies, including 1D simulations, [38][39][40] 2D simulations, 41 3D simulations with rigid walls in idealised geometries, [42][43][44][45][46][47] 3D simulations with rigid walls in more realistic geometries, [48][49][50][51][52][53][54][55] and simulations with distensible walls. 56 Of these studies, several investigated flow unsteadiness.…”