Mechanisms of neointimal formation at sites of restenosis after coronary stenting

冠状动脉支架术后再狭窄仍然是一个重要的临床问题。以往的实验动物研究表明，冠状动脉支架置入术可诱导新生内膜增殖。然而，人类冠状动脉支架术后再狭窄的机制仍不清楚。我们已报道，冠状动脉支架内再狭窄时观察到的同心层新生血管和巨噬细胞聚集可能是血栓形成的组织过程的结果(Komatsu R，Ueda M等)。循环98：224-233,1998。)本研究表明，支架植入后早期新生内膜中存在糖蛋白(GP)IIb/IIIa阳性的血小板血栓(循环100，I-691,1999)。此外，本研究还发现，在人类冠状动脉支架术后早期，血小板活化、P-选择素阳性的血小板聚集和P-选择素介导的中性粒细胞聚集是显著的变化。观察还表明，这些现象触发了修复过程，最终可能导致新生内膜的形成。

Restenosis after coronary stenting remains a significiant clinical problem. Previous experimental animal studies have shown that coronary stenting induces neointimal proliferation. However, the mechanisms that underlie restenosis after coronary stenting in humans are still unclear.We have previonsly reported that the formation of a concentric layer of neovascularization and macrophage accumulation observed at in-stent restenosis in human coronary arteries could result from organization processes of thrombosis (Komatsu R, Ueda M, et al. Circulation 98 : 224-233, 1998.)The present study demonstrates that glycoprotein (GP) IIb/IIIa positive platelet thrombus was present in the neointima at early stages after stenting (Circulation 100, I-691, 1999). The present study, moreover, revealed that platelet activation, P-selectin-positive platelet aggregation, and P-selectin-mediated neutrophil accumulation were prominent changes in the early stages of human coronary arteries after stenting. The observations also suggests that these phenomena trigger the repair process, eventually this may lead to neointimal formation.