Purpose: To determine why some vein grafts fail, we prospectively stud
ied the relationship between the histologic condition of the greater s
aphenous vein (GSV) at the time of grafting and subsequent stenosis of
the vein graft. Methods: Ninety-four remnant segments of GSVs were ob
tained at the time of infrainguinal bypass in 91 patients and were per
fusion fixed before histologic and ultrastructural examination. All by
pass grafts were evaluated clinically and by duplex ultrasonography at
regular intervals from 1 to 30 months after operation. All 24 grafts
that developed lesions that caused thrombosis (failed grafts) or flow
reduction (failing grafts) underwent arteriography and appropriate ope
rative or other interventional correction of the causative lesion. Res
ults: There was no significant difference in the incidence of coronary
artery disease, kidney disease, hypertension, or history of smoking i
n patients with normally functioning and failed or failing grafts. Dia
betes occurred with an increased frequency in failed or failing grafts
(p = 0.056). At the time of their insertion, GSVs that subsequently d
eveloped significant lesions had thicker walls (0. 72 +/- 0.33 mm) com
pared with normally functioning grafts (0.58 +/- 21 mm; p < 0.02). Mos
t of this difference was related to a significantly thicker intima (0.
27 +/- 0.17 vs 0.11 +/- 0.7 mm; p < 0.0001). Another significant findi
ng was the presence of subendothelial spindle-shaped cells greater tha
n five cell layers thick. This occurred more often in pregraft biopsie
s from grafts that developed significant lesions (70.4% vs 7.5%, p < 0
.0001). Electron microscopic examination of these cells demonstrated a
subpopulation of poorly differentiated cells with few fibers and many
vesicles. Four of 24 (17%) failed or failing grafts had evidence of v
ein wall calcification at the time of vein grafting. This was seen in
only one (1.4%) of 70 normally functioning grafts without lesions (p <
0.005). Conclusions: We conclude that GSVs with thick and calcified w
alls or hypercellular intima at the time of grafting are at increased
risk of developing intragraft lesions that may lead to graft failure.
Frequent duplex ultrasonography surveillance is particularly warranted
for such high-risk grafts.