Vein grafts fail because of the development of intimal hyperplasia and athe
roma. Recent experimental evidence suggests that the presence of hyperchole
sterolemia induces a three-fold increase in intimal hyperplasia with early
atheroma development within 4 weeks of implantation. We have previously dem
onstrated endothelial cell preservation and a short-lived (3-day) polymorph
onuclear leukocyte infiltrate in vein grafts. The aim of this study is to d
efine the early morphology and ultrastructure of vein grafts implanted into
a hyperlipidemic environment to provide a pathological foundation on which
to examine the cellular and molecular events that determine this accelerat
ed response. Twenty-one male New Zealand White rabbits underwent a right ca
rotid interposition bypass graft using the ipsilateral external jugular vei
n; all animals received a 1% cholesterol diet for 4 weeks prior to surgery
and continuing postoperatively until harvest. Animals (n = 3 per time point
) were sacrificed at 60 min, 1 day, 3 days, 5 days, 7 days, 14 days, and 28
days postoperatively for scanning and transmission electron microscopy of
the vein grafts. No concurrent controls were employed. The results of this
study suggest that in the presence of hypercholesterolemia, the pathophysio
logical processes involved in the vein graft are similar to those reported
for noncholesterol-fed animals. There is a sustained subendothelial respons
e with the prolonged presence of macrophages and cellular debris and the ac
cumulation of foam cells.