Cardiac Allograft Vasculopathy: Differences in De Novo and Maintenance Heart Transplant Recipients

Abstract

Advances in immunosuppressive therapies in the past decade have improved short-term survival following heart transplantation, but cardiac allograft vasculopathy (CAV) has remained a major cause of mortality and morbidity in the long-term. CAV is often underdiagnosed by coronary angiography; intravascular ultrasound (IVUS) is currently the gold standard for diagnosis of CAV, with an increase in maximal intimal thickness of ≥0.5 mm from baseline to one year post-transplant representing a risk factor for the incidence of cardiac events during follow-up. Non-invasive tests such as stress echocardiography or scintigraphy evaluate the impact of CAV on myocardial function and/or perfusion. They provide useful prognostic information and may serve as screening tests for selecting patients who need invasive evaluation. The need for effective strategies to prevent CAV, and control its progression once established, is of utmost importance to improve long-term survival and quality of life after heart transplantation. Proliferation signal inhibitors (PSIs) have been demonstrated to slow the development of CAV and to reduce the rate of cardiac events in de novo heart transplant recipients. In maintenance patients, palliation of the disease with percutaneous revascularization is being attempted with increasing frequency, with satisfactory short-term success and possible but unproven long-term benefit. A pilot, single-center, randomized study with sirolimus versus standard care suggests that PSIs may also be effective in limiting the progression of established CAV, validating the need for this hypothesis to be explored in larger trials.