Cardiac allograft vasculopathy (CAV) represents the leading cause of late morbidity and mortality in heart transplant recipients and accounts for a second of all-cause mortality at 3 years. Development of CAV is a complex process involving intimal thickening, atherosclerosis, thrombosis and vasculitis by histology, but ultimately, intimal hyperplasia is the predominant cause of lumen narrowing, leading to ischemia and graft failure. In distinction from general coronary atherosclerosis, which is marked by focal and eccentric fibrofatty atheroma, CAV affects diffusely the entire coronary vasculature with marked intimal proliferation and concentric vascular thickening and fibrosis.