Cardiac allograft vasculopathy – problem and model

Cardiac allograft vasculopathy (CAV) is an accelerated form of atherosclerosis induced by immunological endothelial injury with subsequent inflammatory repair responses in a milieu of additional non-immunological risk factors. It is the leading cause of death beyond the first year after transplantation. The clinical situation is characterized by a poorly controlled complexity of pathogenetic and protective mechanisms and the heterogeneous nature concerning functional and structural manifestations, disease progression and prognosis. An early risk prediction algorithm for CAV is required in order to establish optimized preventive and therapeutical strategies. Experimental animals serve as model systems to selectively investigate different steps of the injury cascade providing specific insights into key mechanisms operating in CAV. Beyond its importance in transplantation medicine, human CAV can be taken as an unique model of atherosclerosis allowing evaluation and correlation of vascular function and morphology with the humoral and intracardiac activity/expression of mediators of the disease. Thus, CAV, beyond being a cumbersome clinical problem, represents an unique and attractive model of atherosclerosis in humans offering perspectives beyond the usual.