Kounis Nicholas G, Koniari Ioanna, Roumeliotis Anastasios, Tsigkas Grigorios, Soufras George, Grapsas Nicholas, Davlouros Periklis, Hahalis George
Department of Cardiology, University of Patras Medical School, Patras, Rion, Achaia, Greece.
J Thorac Dis. 2017 Apr;9(4):1155-1164. doi: 10.21037/jtd.2017.03.134.
Percutaneous transluminal coronary angioplasty with coronary stent implantation is a life-saving medical procedure that has become, nowadays, the most frequent performed therapeutic procedure in medicine. Plain balloon angioplasty, bare metal stents, first and second generation drug-eluting stents, bioresorbable and bioabsorbable scaffolds have offered diachronically a great advance against coronary artery disease and have enriched our medical armamentarium. Stented areas constitute vulnerable sites for endothelial damage, endothelial dysfunction, flow turbulence, hemorheologic changes, platelet dysfunction, coagulation changes and fibrinolytic disturbances. Implant surface attracts several proteins such as albumin, fibronectin, fibrinogen, and complement that lead to complement system activation. Macrophages recognize the implant as foreign substance due to protein adsorption and its continuous presence results in macrophage differentiation and fusion into foreign body giant cells. Polymer coating, stent metallic platforms and the released drugs can act as strong antigenic complex that apply continuous, repetitive, persistent and chronic hypersensitivity irritation to the coronary intima. The concomitant administration of oral antiplatelet drugs and environmental exposures can induce hypersensitivity inflammation. A class of platelets, activated via high-affinity and low-affinity IgE hypersensitivity receptors FCγRI, FCγRII, FCεRI and FCεRII, can induce Kounis hypersensitivity-associated thrombotic syndrome inside the stented coronaries. Type III variant of this syndrome is diagnosed when coronary artery stent thrombosis is associated with thrombus infiltrated by eosinophils or mast cells and/or when coronary intima, media and adventitia adjacent to stent, is infiltrated by eosinophils or mast cells. Careful history of hypersensitivity reactions to all implanted materials and concomitant drugs with monitoring of inflammatory mediators as well as lymphocyte transformation studies to detect hypersensitivity must be undertaken in order to avoid disastrous consequences. Food and Drug Administration recommendations for coronary stent implantation should be applied also to bioresorbable scaffolds. Further studies with inert and non-allergenic implants are necessary.
经皮腔内冠状动脉成形术及冠状动脉支架植入术是一种挽救生命的医疗程序，如今已成为医学上最常实施的治疗手段。普通球囊血管成形术、裸金属支架、第一代和第二代药物洗脱支架、生物可吸收和生物可吸收支架，随着时间的推移，在对抗冠状动脉疾病方面取得了巨大进展，并丰富了我们的医疗手段。支架置入区域是内皮损伤、内皮功能障碍、血流紊乱、血液流变学改变、血小板功能障碍、凝血变化和纤溶紊乱的易损部位。植入物表面会吸附多种蛋白质，如白蛋白、纤连蛋白、纤维蛋白原和补体，从而导致补体系统激活。巨噬细胞由于蛋白质吸附而将植入物识别为异物，其持续存在会导致巨噬细胞分化并融合成异物巨细胞。聚合物涂层、支架金属平台和释放的药物可作为强大的抗原复合物，对冠状动脉内膜施加持续、反复、持久和慢性的超敏反应刺激。口服抗血小板药物的同时使用和环境暴露可诱发超敏反应性炎症。一类通过高亲和力和低亲和力IgE超敏反应受体FCγRI、FCγRII、FCεRI和FCεRII激活的血小板，可在置入支架的冠状动脉内诱发库尼斯超敏反应相关血栓形成综合征。当冠状动脉支架血栓形成与嗜酸性粒细胞或肥大细胞浸润的血栓相关，和/或当支架附近的冠状动脉内膜、中膜和外膜被嗜酸性粒细胞或肥大细胞浸润时，可诊断为此综合征的III型变体。必须仔细询问对所有植入材料和伴随药物的过敏反应病史，并监测炎症介质以及进行淋巴细胞转化研究以检测超敏反应，以避免灾难性后果。美国食品药品监督管理局关于冠状动脉支架植入的建议也应适用于生物可吸收支架。有必要对惰性和无致敏性的植入物进行进一步研究。
