Increased expression of ICAM-1 in a case of accelerated coronary artery disease after heart transplantation.

The development of accelerated coronary artery disease after heart transplantation remains the limiting factor for long-term survival. The most widely accepted hypothesis to explain the development of this vascular lesion is chronic immunologic injury to the vessel wall, which leads to recruitment of monocytes and lymphocytes into the intima and to subsequent neointimal proliferation. In this report, we describe a case of accelerated coronary artery disease that led to allograft failure and repeat heart transplantation 3 years after the initial procedure. Pathologic examination showed striking intimal proliferation with abundant expression of intercellular adhesion molecule-1 in both endothelial cells and cells deep within the intima. Cardiac myocytes also stained for intercellular adhesion molecule-1, with the most intense staining noted in intercalated disks, whereas staining for E-selectin was restricted to endothelial cells. These findings are similar to those we observed in a canine model of transplant arteriopathy and highlight the need for further studies to examine whether inhibitors of endothelial cell adhesion molecules or their leukocyte ligands can successfully ameliorate transplant vasculopathy.