Restenosis after arterial angioplasty: a hemorrheologic response to injury.
Restenosis after arterial angioplasty: a hemorrheologic response to injury.
复制标题
动脉血管成形术后再狭窄：对损伤的血液流变学反应。
DOI：
10.1016/0002-9149(87)90477-2
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发表时间：
1987
期刊：
影响因子：
--
通讯作者：
Fuster,V
中科院分区：
文献类型：
--
作者：
Chesebro,JH;Lam,JY;Badimon,L;Fuster,V
动脉血管成形术后的再狭窄似乎是对深动脉损伤的反应，深动脉损伤比浅表损伤（内皮剥脱）更容易形成血栓。深部动脉损伤使胶原蛋白、弹性蛋白和平滑肌细胞暴露于循环血液，释放组织凝血活酶，并由于血小板和凝血系统的激活而导致立即血小板血栓沉积，这两者相互促进对方的激活。内皮细胞的再生也能防止血小板沉积。血小板对胶原蛋白的粘附，以及对深度损伤的动脉壁的粘附，随着剪切速率的增加而增加（与管腔横截面积的四次方成反比，与血流量成正比）；因此，剪切速率的影响增加了手术时充分扩张的重要性。减少急性血小板血栓沉积的治疗似乎是减少再狭窄的重要因素。动脉血管成形术后，在扩张段近端和远端的动脉段中实验性地发生血管收缩，其中没有平滑肌细胞坏死。血管收缩与血小板沉积的严重程度直接相关，可以通过使用小剂量阿司匹林（每天1mg/kg）减少血小板沉积来减少血管收缩，并且可能是由血小板中的血管收缩物质（血栓素A2、血清素和其他物质）介导的。这些物质的血小板膜受体抑制剂可减少血管收缩，但不会减少血小板沉积。治疗干预可能应该包括抗凝和血小板抑制。血小板膜受体对纤维蛋白原受体、因子 VIII-血管性血友病因子或两者的抑制对于充分减少急性血小板血栓沉积可能是必要的。
Restenosis after arterial angioplasty appears to be a response to deep arterial injury, which is much more thrombogenic than superficial injury (endothelial denudation). Deep arterial injury exposes collagen, elastin and smooth muscle cells to circulating blood, releases tissue thromboplastin and causes immediate platelet-thrombus deposition as a result of activation of platelets and the clotting system, both of which mutually facilitate activation of the other. Regrowth of endothelium also is protective against platelet deposition. Platelet adherence to collagen, and thus to the arterial wall that is deeply injured, increases with shear rate (related inversely to the fourth power of luminal cross-sectional area and directly to blood flow); thus, the effect of shear rate increases the importance of adequate dilatation at the time of the procedure. Therapy that will reduce acute platelet-thrombus deposition appears to be an important factor for reduction of restenosis. Vasoconstriction occurs experimentally after arterial angioplasty in arterial segments proximal and distal to the dilated segment where there has been no necrosis of smooth muscle cells. The vasoconstriction is directly related to the severity of platelet deposition, can be reduced by reducing platelet deposition with low dose aspirin (1 mg/kg daily) and is probably mediated by vasoconstrictor substances from platelets (thromboxane A2, serotonin and other substances). Platelet-membrane receptor inhibitors to these substances reduce the vasoconstriction but do not reduce platelet deposition. Therapeutic intervention should probably involve both anticoagulation and platelet inhibition. Platelet-membrane receptor inhibition to the fibrinogen receptor, factor VIII-von Willebrand factor or both may be necessary acutely to sufficiently reduce acute platelet-thrombus deposition.