Pathogenesis of Cardiac Allograft Vasculopathy (Chronic Rejection)

Despite the dramatic improvement of early and 1-year survival following cardiac transplantation, long-term mortality has not been substantially impacted[1]. The major cause of late mortality is an accelerated obliterative coronary artery disease, presumably a manifestation of chronic rejection[2], which will be referred to in this review as cardiac allograft vasculopathy (CAV). The incidence of CAV is between 10% and 15% per year, with a prevalence of as high as 45% at 5 years based on angiographic diagnosis[3]. With the more sensitive intravascular ultrasound, some investigators have reported virtually 100% prevelance of the disease[4]. This review will focus on the pathophysiology and im munologic mechanisms proposed for CAV, as well as current diagnostic and potential therapeutic interventions for the disease.