ABSTRACT
The removal of a venous conduit from its bed subjects it to the cumulative injurious effects of surgical manipulation, transmural warm ischemia, contact with nonhemic solutions, and hydrostatic dilatation.[1] With the rapid increase in aortocoronary and infrainguinal vein grafting as the stimulus for the evaluation of these injuries,[2,3] it has now been shown that there is widespread destruction of the endothelium with alterations in normal prostacylin and thromboxane production, thus producing a relatively thrombogenic surface. Furthermore, the rate of degeneration in such veins appears to be inversely related to the subsequent rate of flow.[4]
All these factors may contribute to the initial failure rate of these bypass conduits, particularly when the outflow tracts are limited.[5] Although the most recent methods of preparing excised vein grafts have been directed toward the prevention of these injuries,[6] none is perfect. At present we believe that the closest approximation to an ideal conduit (i.e., one with normal, viable, physiologically functioning endothelium and a natural taper) is a vein that has been retained in situ and is minimally damaged during its preparation for bypass.
