Short-term survival of cardiac allografts has increased markedly because of surveillance by protocol endomyocardial biopsies and improvements in immunosuppression, which have largely prevented graft loss from acute rejection. Currently, 85% of allograft recipients survive for 1 year, and 70% can expect to survive 5 years.1 Despite this progress, chronic cardiac allograft arteriopathy (also known as chronic rejection, graft vascular disease, or accelerated atherosclerosis) remains a substantial and intractable obstacle to long-term survival, accounting for 21% to 30% of deaths.2,3 The other major complications relate to the immunosuppression treatment itself (malignancy, infections).
See also p 1169.
Although graft atherosclerotic disease shares certain aspects with native coronary atherosclerosis, including dysfunctional endothelium with subsequent endothelial—inflammatory cell interaction, there are significant differences in the morphology, distribution, and most certainly pathogenesis.4 The introduction of intravascular ultrasound has also shown that the process is much more prevalent and occurs earlier than had been
Aretz HT, Colvin RB. Endomyocardial BiopsiesAn Early Warning System for Chronic Transplant Arteriopathy. JAMA. 1997;278(14):1197-1198. doi:10.1001/jama.1997.03550140089048