Cardiac allograft vasculopathy (CAV) is a unique form of accelerated atherosclerosis that represents the main late cause of morbidity and mortality, affecting almost half patients at ten years after heart transplantation (HTx). Unless the pathogenesis of CAV is still not completely understood, it seems to be the result of a complex interplay between immunological and non-immunological factors that induce endothelial injury. Histologically epicardial and intramural vessels present a concentric circumferential intimal thickening caused by smooth muscle cell proliferation, inflammatory cells, and lipid deposition. Coronary angiography is still considered the gold-standard diagnostic tool for CAV detection but has reduced sensibility due to its inability to visualize beyond the arterial lumen. Intravascular ultrasound (IVUS) allows detecting early intimal thickening with high sensitivity. Plaque composition and vulnerability, detectable with virtual histology (VH/IVUS), and optical coherence tomography (OCT) seem to relate to adverse clinical events. Treatment approaches continue to evolve, but prevention and early detection remain the focus. Mammalian target of rapamycin inhibitors can significantly delay the development and the progression of CAV, but their optimal use remains to be established. New encouraging results come from monoclonal autoantibodies. At present percutaneous revascularization procedures seem to have only a palliative meaning, with no clear evidence of survival advantage over medical therapy and should be considered in case of a focal disease. Drug-eluting stents have proven to reduce in-stent restenosis, with a potential role of imaging-guided intervention in this setting. Heart re-transplantation is the only resolutive therapy and is considered in the case of CAV associated with graft dysfunction.
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