Early morphology of accelerated vein graft atheroma in experimental vein grafts

Vein grafts fail because of the development of intimal hyperplasia and atheroma. Recent experimental evidence suggests that the presence of hypercholesterolemia induces a three-fold increase in intimal hyperplasia with early atheroma development within 4 weeks of implantation. We have previously demonstrated endothelial cell preservation and a short-lived (3- day) polymorphonuclear leukocyte infiltrate in vein grafts. The aim of this study is to define 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 accelerated response. Twenty-one male New Zealand White rabbits underwent a right carotid interposition bypass graft using the ipsilateral external jugular vein; 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 pathophysiological processes involved in the vein graft are similar to those reported for noncholesterol-fed animals. There is a sustained subendothelial response with the prolonged presence of macrophages and cellular debris and the accumulation of foam cells.