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