title: Coronary restenotic reduction of drug-eluting stenting may be due to its anti-inflammatory effects.
abstract: The development of coronary stent has revolutionized the field of interventional cardiology by reducing the incidence of restenosis after balloon angioplasty. However, the stent has still associated with a serious complication, namely, in-stent restenosis. Although, restenosis following coronary stenting has long been attributed to neointimal proliferation, thrombosis, and negative remodeling, the inflammation may be a trigger for those vascular reactions following coronary stenting. Both experimental and clinical studies have demonstrated a marked activation of local and systemic inflammatory response following stent implantation, suggesting that inflammation may play an important role in determining in-stent restenosis via neointimal proliferation. The key role of inflammation in vascular healing and in-stent retsenosis has also been increasingly well understood. Recently, drug-eluting stents (DESs) have been shown to decrease in-stent restenosis in a large number of clinical studies. In addition to their anti-proliferative activity, DESs have been considered to possess an anti-inflammatory property, especially for sirolimus-eluting stent compared with bare metal stent. Moreover, the benefit of the anti-inflammatory therapy during the peri-procedural period and long-term follow-up by means of drug administration is also dependent on the inflammatory status during percutaneous coronary intervention. Measurement of cytokine and acute phase proteins, such as C-reactive protein, therefore, may be important to identify high-risk subjects and develop specific treatment tailored to the individual patients with stent restenosis. Thus, therapeutic approach should be further directed toward increasing local resistance to proliferative inflammatory stimuli by means of anti-proliferative, locally delivered drugs and reducing the magnitude and persistence of systemic inflammation.
authors.affiliation: Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Science, Peking Union Medical College, Beijing 100037, PR China. lijnjn@yahoo.com
authors.forename: Jian-Jun
authors.initials: JJ
authors.lastname: Li
authors.forename: Jie
authors.initials: J
authors.lastname: Li
authors.forename: Jin-Lo
authors.initials: JL
authors.lastname: Nan
authors.forename: Zhen
authors.initials: Z
authors.lastname: Li
authors.forename: Xin
authors.initials: X
authors.lastname: Zhen
authors.forename: Chao-Wei
authors.initials: CW
authors.lastname: Mu
authors.forename: Jun
authors.initials: J
authors.lastname: Dai
authors.forename: Chao-Yang
authors.initials: CY
authors.lastname: Zhang
mesh_terms: D000893:Anti-Inflammatory Agents / Q000008:administration & dosage* / Q000276:immunology; D001807:Blood Vessel Prosthesis / Q000009:adverse effects*; D023903:Coronary Restenosis / Q000209:etiology / Q000276:immunology* / Q000517:prevention & control*; D054855:Drug-Eluting Stents / Q000009:adverse effects*; D006083:Graft Occlusion, Vascular / Q000276:immunology* / Q000517:prevention & control*; D006801:Humans; D008955:Models, Cardiovascular; D018448:Models, Immunological
chemical_list: D000893:Anti-Inflammatory Agents