Cardiac allograft vasculopathy (CAV) is a major long-term complication of h
eart transplantation. Coronary endothelial injury provokes immunological re
actions leading to inflammation and proliferation of vascular smooth muscle
cells. Recent studies suggest that cell death of endothelial cells during
early phases of transplant arteriopathy development proceeds via programmed
cell death (apoptosis). The potential role of apoptosis in CAV is discusse
d. Based on these concepts, therapeutic strategies might be envisaged aimed
at the prevention of apoptosis during the initiating phase of CAV.