PET Assessment of Cardiac Allograft Vasculopathy After Heart Transplantation

Cardiac allograft vasculopathy (CAV) remains 1 of the leading causes of late mortality beyond the first year after heart transplantation (HT).1 Despite advances in immunosuppressive therapy and risk factor control, CAV progression remains a devastating complication in many HT recipients, ultimately leading to graft failure and adverse cardiac events. According to the ISHLT (International Society for Heart and Lung Transplantation) registry data, the incidence of CAV remains high, with minimal reduction over the past 2 decades, from 32% to 29% at 5 years after HT.1 Furthermore, the 5-year survival of patients with diagnoses of CAV within 3 years of HT has improved only marginally (from 71% to 76%) and remains considerably lower than the 82% survival rate for patients without CAV.1 A further understanding of its pathophysiology and the development of efficient methods for early diagnosis and treatment of CAV are therefore pivotal for improving outcomes Due to HT denervation, the clinical manifestations of CAV are generally silent or atypical, including the development of overt heart failure complicating allo