Inhibitory effect of brachytherapy on intimal hyperplasia in arteriovenous fistula

Purpose. To determine whether endovascular radiation can inhibit intimal hyperplasia in a swine model of hemodialysis access. Materials and methods. Polytetrafluoroethylene arteriovenous grafts (6 mm in diameter) were placed between the common carotid artery and the external jugular vein bilaterally in 8 pigs. Two days after the surgery, fistulography was performed. Gamma radiation (12 Gy) was delivered endovascularly to one of the grafts at the venous anastomosis by using an iridium¹⁹² source. Thus, the other graft in each pig served as an untreated control. Fistulas were evaluated with fistulography or venography 6 week after radiation. All grafts were then harvested for histological and immunohistochemical examination. Results. Seven grafts on the treated side and 5 grafts on the control side remained patent for at least 6 weeks. Angiography demonstrated that the percentage stenosis at the venous anastomosis was significantly lower for the treated group (15.9 ± 14.1 versus 32.6 ± 16.7%, P = 0.045). Histopathologic analyses revealed that the mean intimal area and maximal intimal thickness were significantly lower with reduced smooth muscle cell proliferation at the venous anastomosis on the treated side compared to the control side (0.68 ± 0.30 versus 1. 06 ± 0.29 mm², P = 0.017, and 0.18 ± 0.08 versus 0.26 ± 0.07 mm, P = 0.004, respectively). The residual lumen was significantly greater for the treated group (1.59 ± 0.42 versus 1.06 ± 0.37 mm², P = 0.031). No significant differences were found in the area, nor maximal thickness in the vein either proximal or distal to the anastomosis between the two groups. Conclusions. In an animal model of hemodialysis access, brachytherapy with iridium¹⁹² delivered 2 days after graft implantation reduces intimal hyperplasia and stenosis at the venous anastomosis. The reduced smooth-muscle cells found in the radiated veins suggests that brachytherapy may exert its effect on neointimal formation by inhibition of smooth muscle cell proliferation.