The clinical dilemma of cardiac allograft vasculopathy – an introduction to the clinical session

Abstract

Cardiac allograft vasculopathy is the major long-term problem after heart transplantation. However, the assumption, mostly based on experimental animal data, that human CAV is an immune-mediated diffuse concentric intimal proliferation with progressive, homogenous vessel narrowing, involving equally epicardial arteries and the microcirculation, leading inevitably to ischemic organ failure and death, does not adequately reflect the complexity of the clinical setting. CAV in humans is much more characterized by a very heterogeneous pattern concerning pathogenetic mechanisms (e.g., immune activation, ischemia-reperfusion injury, CMV infection, hyperlipoproteinemia), protective mechanisms (e.g., remodeling, endothelium-derived vasodilators), endothelial dysfunction, morphological manifestations, involvement of the microcirculation, temporal appearance, disease progression and prognosis. Thus, clinicians have to deal with several clinical dilemmas of the disease, which can be summarized in three simple questions: how can CAV be detected/diagnosed, how can CAV and related events be predicted, and finally how can CAV be prevented and treated. Initial and promising answers to these pivotal questions have been found in recent years, and continuing progress is under way.