title: [Restenosis following endovascular interventions: clinical and experimental studies].
abstract: Restenosis following endovascular interventions is the main limitation of their long-term success. The incidence of restenosis varies according to the method (stenting, endarterectomy) and the treated vascular region, but the pathomechanism and risk factors are similar. The current article reviews of the author's previous studies in this field. In clinical studies, we compared the restenosis rate after carotid artery stenting and carotid endarterectomy. We also analyzed the complement activation profile after these interventions. In another study, we investigated the role of two polymorphisms of the estrogen receptor alpha in the occurrence of carotid restenosis after either carotid artery stenting or carotid endarterectomy. In an animal model of carotid endarterectomy, we studied the role of the nitrite-oxide-cyclic guanosine monophosphate signaling and the effect of the phosphodiesterase-5 inhibitor therapy in neointimal hyperplasia. Our results suggest that higher incidence of restenosis following carotid endarterectomy can be correlated with the more highly expressed complement activation after this type of carotid intervention. Polymorphisms in the estrogen receptor alpha gene could contribute to the restenosis formation, especially in women. Neointimal hyperplasia can be attenuated by increased cyclic guanosine monophosphate signaling.
authors: Semmelweis Egyetem, Altalános Orvostudományi Kar, Kardiológiai Központ, Budapest Gaál József u. 9. 1122. hirschbergkristof@gmail.com
authors: Kristóf
authors: K
authors: Hirschberg
authors: László
authors: L
authors: Entz
authors: Gábor
authors: G
authors: Szabó
authors: Béla
authors: B
authors: Merkely
mesh_terms: D000818:Animals; D002339:Carotid Arteries / Q000378:metabolism / Q000473:pathology* / Q000601:surgery*; D003167:Complement Activation; D006152:Cyclic GMP / Q000378:metabolism; D016894:Endarterectomy, Carotid; D047628:Estrogen Receptor alpha / Q000235:genetics; D005260:Female; D006083:Graft Occlusion, Vascular / Q000175:diagnosis / Q000378:metabolism / Q000517:prevention & control / Q000628:therapy; D006801:Humans; D006965:Hyperplasia / Q000378:metabolism; D015994:Incidence; D008297:Male; D058986:Phosphodiesterase 5 Inhibitors; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011110:Polymorphism, Genetic; D051381:Rats; D012189:Retrospective Studies; D015398:Signal Transduction; D015607:Stents; D017539:Tunica Intima / Q000378:metabolism / Q000473:pathology; D014654:Vascular Patency
chemical_list: D047628:Estrogen Receptor alpha; D058986:Phosphodiesterase 5 Inhibitors; D010726:Phosphodiesterase Inhibitors; D006152:Cyclic GMP