Zotz R J, Dietz U, Lindemann S, Genth-Zotz S
Marienhaus Klinikum Eifel, Krankenhausstr. 1, 54634, Bitburg, Deutschland.
DKD Helios Klinik Wiesbaden, Wiesbaden, Deutschland.
Herz. 2019 Feb;44(1):35-39. doi: 10.1007/s00059-018-4777-0.
Coronary restenosis is the answer of the arterial wall to a mechanical violation through balloon angioplasty, bare-metal (BM) stent implantation or rotational atherectomy through repeated narrowing. It has great clinical and prognostic relevance and occurs in approximately 30% of non-coated stents and in 10% of coated coronary stents. The wound healing process that precedes restenosis includes inflammatory reactions, cellular proliferation and remodeling of the arterial wall, where protein synthesis of the extracellular matrix is initiated. The inflammatory reaction activates platelets, leucocytes and monocytes and stimulates smooth muscle cells. The medications on the drug-eluting stents (rapamycin, paclitaxel, sirolimus, evarolimus and zotarolimus) inhibit cell division, are cytotoxic and only these sustainably influence restenosis. Whether they play a role in neoatherosclerosis needs to be determined. The mechanism of restenosis with implantation of drug-eluting stents is heterogeneous and associated with the deposition of T‑lymphocytes and fibrin. Risk factors for the development of restenosis include mechanical factors, such as incorrect apposition and expansion of stents, inflammation, diabetes mellitus, genetic factors, bypass operations, stent length and stent diameter. The restenosis rate is lower with drug-eluting stents and must be considered differently between the drug-eluting stents. Drug-eluting stents of the latest generation and drug-coated balloons (DCB) showed the best clinical and angiographic results for in-stent restenosis in randomized trials. The BM and older first-generation drug-eluting stents should be avoided. Further randomized studies are needed.
冠状动脉再狭窄是动脉壁对球囊血管成形术、裸金属（BM）支架植入或旋磨术等机械性损伤的反应，通过反复狭窄而发生。它具有重大的临床和预后相关性，约30%的无涂层支架和10%的涂层冠状动脉支架会出现这种情况。再狭窄之前的伤口愈合过程包括炎症反应、细胞增殖和动脉壁重塑，在此过程中启动细胞外基质的蛋白质合成。炎症反应激活血小板、白细胞和单核细胞，并刺激平滑肌细胞。药物洗脱支架（雷帕霉素、紫杉醇、西罗莫司、依维莫司和佐他莫司）上的药物抑制细胞分裂，具有细胞毒性，只有这些药物能持续影响再狭窄。它们是否在新生动脉粥样硬化中起作用尚待确定。药物洗脱支架植入后再狭窄的机制是异质性的，与T淋巴细胞和纤维蛋白的沉积有关。再狭窄发生的危险因素包括机械因素，如支架贴壁和扩张不当、炎症、糖尿病、遗传因素、搭桥手术、支架长度和支架直径。药物洗脱支架的再狭窄率较低，不同药物洗脱支架之间的情况必须区别对待。在随机试验中，最新一代的药物洗脱支架和药物涂层球囊（DCB）在支架内再狭窄方面显示出最佳的临床和血管造影结果。应避免使用BM支架和较旧的第一代药物洗脱支架。还需要进一步的随机研究。
