脑血管支架置入后的血流动力学变化

Hemodynamic changes following cerebrovascular stenting

血管支架作为一种异物,置入后引起血小板-单核细胞聚集体,调整单核细胞的许多行为,诱导单核细胞表达组织因子,促进血管损伤部位血栓内部纤维蛋白的沉积,在支架置入后血管壁损伤的炎症反应中有促进作用。还可以刺激血小板在血管支架表面聚集、激活血小板系统及凝血系统,导致血栓形成。平滑肌细胞向损伤部位迁移发生增殖反应,新生内膜大量增生,血管壁重构引起支架内再狭窄。血管支架置入后发生支架内再狭窄的影响因素不仅取决于支架种类,而且还取决于宿主原有的疾病,此外,血管支架置入前狭窄的严重程度以及支架置入后残留狭窄的长度等都会对再狭窄产生影响。抑制血管内膜过度增生或改善新生内膜形成以及血管重塑过程均可有效防止再狭窄。

Intravascular stent as a foreign body induces platelet-monocyte aggregation following implantation, mediates various actions of monocyte, induces monocyte to express tissue factors, promotes fibrin sedimentation at injury site, and accelerates inflammatory reaction of vessel wall injury. In addition, it stimulates platelet aggregation on the stent, activates platelet system and coagulation system, resulting thrombosis. Smooth muscle cells migration to injury site, neointima hyperplasia, and vessel wall reconstruction cause in-stent restenosis. The influential factors that induce restenosis include type of stent, original diseases of the host, stenosis severity before stenting and residual stenosis length after stenting. Inhibition of tunica intima hyperplasia or improvement of neointima as well as vessel wall reconstruction could effectively prevent restenosis.