Delayed re-endothelialization and T-cell infiltration following intracoronary radiation therapy in the porcine model

Purpose: To evaluate the late induction of apoptosis following intracoronar y radiation (IR) and the effects of IR on inflammatory cells. Methods and Materials: Porcine coronaries were injured by balloon overstret ch followed by either 0 or 15 Gy of Ir-192 prescribed to 2 mm from the cent er of the source. Swine were euthanized at 3, 7, and 14 days posttreatment, and arteries were stained for markers of smooth muscle cells (SMCs alpha - actin), T cells (CD3), macrophages, endothelial cells, and apoptotic nuclei (terminal uridine nick end labeling, TUNEL). Intimal area (IA) and IA corr ected for medial fracture length (IA/FL) were quantified by digital image a nalysis, which was also used to quantify the distribution of immunostain-po sitive cells in the adventitia, media, and neointima, respectively. Results: IA/FL was significantly reduced following treatment with 15 Gy, in association with decreased SMC density. Following injury and IR, TUNEL- an d CD3-positive cell density increased significantly, and density of macroph ages was increased in the adventitia and neointima. Staining for endothelia l cells revealed a delay of re-endothelialization after radiation treatment . Conclusion: Increased T-cell infiltration at the medial tear following IR, perhaps due to incomplete reendothelialization, may indicate incomplete hea ling. The elevated apoptosis of these infiltrating T cells may indicate a m echanism for the resolution of inflammation. (C) 2001 Elsevier Science Inc.