Estrogen-eluting, phosphorylcholine-coated stent implantation is associated with reduced neointimal formation but no delay in vascular repair in a porcine coronary model.
Estrogen can inhibit intimal proliferation and accelerate endothelial regeneration after angioplasty. This suggests that estrogen may prevent in-stent restenosis. Unlike other therapies to prevent restenosis, estrogen may also not delay endothelial regrowth, thereby avoiding the risk of late stent thrombosis. The purpose of this work was to determine the effect of a 17beta-estradiol-eluting stent on neointimal formation in a porcine model. Each artery of six pigs was randomized to either a control, low-dose, or high-dose 17beta-estradiol-eluting stent. All animals were sacrificed at 30 days for histopathological analysis. There was a 40% reduction in intimal area in the high-dose stents compared with control stents (2.54 +/- 1.0 vs. 4.13 +/- 1.1 mm(2), for high dose vs. control, respectively; P < 0.05). There was complete endothelial regeneration at 30 days and similar inflammatory response to stenting on histopathology in all the stent groups. This is the first study to show that 17beta-estradiol-eluting stents are associated with reduced neointimal formation without affecting endothelial regeneration in the pig model of in-stent restenosis. Estrogen-coated stents may have a potential benefit in the prevention and treatment of in-stent restenosis.
D000818:Animals; D020099:Coated Materials, Biocompatible; D023903:Coronary Restenosis / Q000473:pathology / Q000517:prevention & control / Q000628:therapy*; D016503:Drug Delivery Systems; D004730:Endothelium, Vascular / Q000473:pathology; D004958:Estradiol / Q000008:administration & dosage* / Q000627:therapeutic use; D023421:Models, Animal; D010767:Phosphorylcholine; D011474:Prosthesis Design; D011897:Random Allocation; D015607:Stents; D013552:Swine
D020099:Coated Materials, Biocompatible; D010767:Phosphorylcholine; D004958:Estradiol