Aortocoronary saphenous vein graft disease, with its increasing clinic
al sequelae, presents an important and unresolved dilemma in cardiolog
ical practice. During the 1st month after bypass surgery, vein graft a
ttrition results from thrombotic occlusion, while later the dominant p
rocess is atherosclerotic obstruction occurring on a foundation of neo
intimal hyperplasia. Although the risk factors predisposing to vein gr
aft atherosclerosis are broadly similar to those recognized for native
coronary disease, the pathogenic effects of these risk factors are am
plified by inherent deficiencies of the vein as a conduit when transpo
sed into the coronary arterial circulation. A multifaceted strategy ai
med at prevention of vein graft disease is emerging, elements of which
include: continued improvements in surgical technique; more effective
antiplatelet drugs; increasingly intensive risk factor modification,
in particular early and aggressive lipid-lowering drug therapy; and a
number of evolving therapies, such as gene transfer and nitric oxide d
onor administration, which target vein graft disease at an early and f
undamental level. At present, a key measure is to circumvent the probl
em of vein graft disease by preferential selection of arterial conduit
s, in particular the internal mammary arteries, for coronary bypass su
rgery whenever possible.