Impact of donor benign intimal thickening on cardiac allograft vasculopathy

We propose that retention of the SMC-rich BIT layer after transplantation accounts, to a large extent, for the donor-derived, SMC-rich nature of human CAV, and that perturbation of the BIT provides the inflammatory foundation for the development of an accelerated atherosclerosis in the epicardial coronaries of transplant patients. This expanding accelerated atherosclerosis along with the underlying BIT demonstrates the characteristics ascribed to CAV.