Li Jian-Jun, Li Jie, Nan Jin-Lo, Li Zhen, Zhen Xin, Mu Chao-Wei, Dai Jun, Zhang Chao-Yang
Department of Cardiology, Fu Wai Hospital, Chinese Academy of Medical Science, Peking Union Medical College, Beijing 100037, PR China.
Med Hypotheses. 2007;69(5):1004-9. doi: 10.1016/j.mehy.2007.01.090. Epub 2007 May 11.
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.
冠状动脉支架的发展通过降低球囊血管成形术后再狭窄的发生率，彻底改变了介入心脏病学领域。然而，支架仍与一种严重并发症相关，即支架内再狭窄。尽管冠状动脉支架置入术后的再狭窄长期以来一直归因于新生内膜增生、血栓形成和负性重塑，但炎症可能是冠状动脉支架置入术后这些血管反应的触发因素。实验和临床研究均表明，支架植入后局部和全身炎症反应会显著激活，这表明炎症可能通过新生内膜增生在决定支架内再狭窄方面发挥重要作用。炎症在血管愈合和支架内再狭窄中的关键作用也越来越为人所理解。最近，大量临床研究表明药物洗脱支架（DESs）可降低支架内再狭窄。除了其抗增殖活性外，DESs被认为具有抗炎特性，尤其是与裸金属支架相比，西罗莫司洗脱支架。此外，在围手术期和长期随访期间通过药物给药进行抗炎治疗的益处也取决于经皮冠状动脉介入治疗期间的炎症状态。因此，测量细胞因子和急性期蛋白，如C反应蛋白，对于识别高危患者以及为支架再狭窄的个体患者制定特定治疗方案可能很重要。因此，治疗方法应进一步朝着通过抗增殖、局部递送药物增加局部对增殖性炎症刺激的抵抗力以及降低全身炎症的程度和持续时间的方向发展。
