Hofstra L, Bergmans DCJJ, Leunissen KML, Hoeks APG, Kitslaar PJEHM, Daemen MJAP, Tordoir JHM
Anastomotic intimal hyperplasia in prosthetic AV fistulas for hemodialysis is associated with initial high flow velocity and not with mismatch in elastic properties

J Am Soc Nephrol (Dec) 6:1625-1633 1995

These studies, conducted at the University Hospital of Maastricht in the Netherlands, address the cause of the almost inevitable stenosis that develops at or just beyond the venous anastomosis in patients with A-V grafts for hemodialysis access. A total of 24 forearm PTFE grafts were followed prospectively for two years with Vessel Wall Doppler Tracking (VWDT), a non-invasive method that uses ultrasound B-mode imaging of blood vessels to record pulsatile changes in cross sectional diameter with time and to record blood flow velocity. This technique measures the time-dependent change in vessel wall diameter and cross sectional area, a stretching response to the pulsatile change in blood pressure at the site of measurement. Measurements in millisecond intervals were taken for 3 to 5 heartbeats immediately proximal and immediately distal to the venous anastomosis to compare differences in elasticity (mismatch) and flow velocity.

Sixteen of the twenty four grafts developed 20 stenoses after a mean of 12.2 months, all at the venous end and all requiring surgical correction. VWDT showed that the graft was less elastic than the attached vein, a mismatch phenomenon that has been blamed for the stimulation of venous intimal and smooth muscle hyperplasia that causes stenosis at the junction. However, in the present study the mismatch in elasticity between graft and vein, expressed as both as a difference in relative distention and in area increase, correlated inversely with the development of stenosis. Patients with larger mismatches, indicating increased strain at the anastomosis, were less likely to develop stenosis (p < 0.05). This finding contrasts sharply with several previous studies in animals and in humans both in vivo and in cultured cells including the authors' own study published one year previously in the same journal, that suggested a role for mechanical stretching and decreased shear stress inducing intimal hyperplasia. The authors' current study also showed that initial peak systolic velocity factored for vessel diameter at the anastomosis (measured within four weeks after surgery) correlated (p < 0.05) with the eventual development of stenosis. They note that this finding is consistent with animal studies that show intimal thickening at the sites of highest flow velocities in A-V grafts presumably due to high shear stresses that causes denudation of the intima. The authors attempt to explain the previous conflicting data on the basis of different experimental conditions. They suggest that animals may react differently than humans and that venous intima may be more susceptible than arterial intima to high velocity forces. Their clinical extrapolations of the data suggest that use of 4 to 7 mm tapered grafts and wide venous cuffs may help to decrease the velocity of flow and resulting shear forces at the venous anastomosis and that use of more compliant elastic grafts may not confer any benefit.

The often confusing and conflicting data regarding factors that predispose to venous stenosis in A-V grafts suggest that we are looking for the answers in the wrong places. This study is most valuable in shedding a negative light on the compliance mismatch hypothesis. Implication of initial peak velocity as a stenosis-causing factor will require confirmatory prospective studies. (Depner)

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Basic hemodialysis : Vascular Access: graft/fistula