Humanizing the problem of transplant vasculopathy.

A frequent problem in transplantation is allograft survival, which can be exacerbated by nonimmune mechanisms in response to perioperative injury of the blood vessels.1 In addition to inflammatory responses, nonimmune mechanisms may also contribute to the development of graft arteriosclerosis (GA), found frequently in cardiac allografts.2 GA of the coronary arteries, or cardiac allograft vasculopathy, is characterized by expansion of the intima and inadequate outward remodeling of the arteries of the graft. Similar pathology is also observed in other solid organ graft types, such as renal allografts.3 It is unclear whether this type of GA is a direct response of the vasculature to injury, including rejection and perioperative injury, or whether it is an indirect response to injury that changes the way the immune system interacts with the graft.