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Recent reports describing late fatal complications after the use of arterial homografts are becoming more numerous.2 Experiences with two recent cases substantiates these reports and strengthens further the argument in favor of plastic arterial substitutes. Much experimental, as well as some clinical, evidence is accumulating that the degeneration in the homograft is proceeding at a far greater rate than similar changes in the host aorta.5The initial changes in the intima, media, and adventitia have been described, but persistence of elastic fibers for years with little degeneration was found to be satisfactory evidence in favor of the freeze-dry aortic homograft.4 In the years to follow, autopsy studies and other reports describing further structural alterations in the homograft were presented.3 Late fragmentation, as well as aneurysmal dilatation at the site of anastomosis, was described.1 The thickened, but weakened, intima and media show evidence of degenerative changes,