Cardiac allograft vasculopathy (CAV) is a significant long-term complication that occurs following heart transplantation, characterized by a progressive, diffuse narrowing of the coronary arteries of the transplanted heart. It is classified as a form of accelerated atherosclerosis and is distinct from typical coronary artery disease due to its unique pathophysiological mechanisms, which are largely driven by alloimmune responses. The definition of CAV encompasses the development of progressive intimal hyperplasia, leading to obstructive lesions that can severely compromise the graft's blood supply, contributing to ischemia and potentially graft failure. The onset of CAV often begins in the first year after transplantation, with prevalence increasing over time, making diligent monitoring essential. The condition is insidious, and patients may remain asymptomatic until significant graft dysfunction occurs, complicating its diagnosis. Clinical manifestations can include angina, heart failure, or myocardial infarction, but many patients may not present with traditional symptoms, which can lead to late detection. Risk factors for developing CAV include older donor age, longer ischemic times, previous rejection episodes, and non-adherence to immunosuppressive regimens. Histological examination of the vascular lesions shows features of both acute and chronic rejection, with evidence of smooth muscle cell proliferation and extracellular matrix deposition within the arterial wall. To monitor for CAV, invasive coronary angiography remains the gold standard; however, non-invasive imaging techniques, such as cardiac magnetic resonance imaging and positron emission tomography, have been valued for providing additional insights without the risks associated with coronary angiography. The management of CAV is challenging, as there is currently no standardized treatment protocol. Strategies may include optimizing immunosuppression, utilizing novel therapies aimed at modifying the immune response, and implementing lifestyle changes to control traditional cardiovascular risk factors. Current research focuses on identifying biomarkers for detecting CAV earlier, improving risk stratification, and enhancing therapeutic interventions. Despite advancements in the understanding of CAV, its impact on long-term outcomes following heart transplantation remains a critical concern, contributing to morbidity and mortality among transplant recipients. As such, ongoing research and clinical trials are imperative to develop more effective prevention and treatment strategies to mitigate the risks associated with CAV and improve the longevity of cardiac allografts. In summary, CAV represents a complex and multifaceted challenge in the post-transplant setting, necessitating a proactive approach in both surveillance and management to ensure optimal outcomes for heart transplant patients.
