Armed Forces Institute of Pathology, Washington, DC, USA.
Pathology. 2010 Jan;42(1):15-22. doi: 10.3109/00313020903434348.
Intraplaque haemorrhage has been shown to be important in necrotic core enlargement. Immunolocalisation of fibrin within progressive stages of plaque progression has not been extensively studied.
Histological sections (n = 74) of human coronary arteries were stained immunohistochemically for fibrin II, red blood cell antigen (glycophorin A), and CD31. Plaques were chosen to represent a range of lesions [6 adaptive intimal thickening, AIT (AHA grade I); 4 intimal xanthomas (AHA grade II), 19 pathologic intimal thickening, PIT (AHA grade III, or pre-atheroma); 34 fibroatheromas, FA (AHA grade IV and V); and 11 thin cap fibroatheromas (TCFA, AHA grade IV)].
Fibrin was generally absent in the intima of AIT and PIT, with moderate staining in cores of early FA (2.6 +/- 0.3). All late FA and TCFA demonstrated intracore fibrin, with mean scores of 2.9 +/- 0.3 and 3.0 +/- 0.3, respectively. Intimal vasa vasorum counts increased with intimal fibrin score (p < 0.0001); in 68% of cores with fibrin staining, there was minimal or no evidence of red cell breakdown.
Fibrin in necrotic cores is present proportional to intraplaque vasa vasorum and before red cells, suggesting leakage of vessels before frank intraplaque haemorrhage. Fibrin may play a role in the bridge between pre-atheroma and atheroma.
已有研究表明,斑块内出血(intraplaque haemorrhage)在坏死核心扩大中起重要作用。在斑块进展的渐进阶段,纤维蛋白的免疫组织化学定位尚未得到广泛研究。
对人冠状动脉的组织学切片(n = 74)进行纤维蛋白 II、红细胞抗原(糖蛋白 A)和 CD31 的免疫组织化学染色。选择斑块以代表一系列病变[6 种适应性内膜增厚(adaptive intimal thickening,AIT)(AHA 分级 I);4 种内膜黄色瘤(intimal xanthomas,AHA 分级 II),19 种病理性内膜增厚(pathologic intimal thickening,PIT)(AHA 分级 III,或动脉粥样前体;atherosclerotic precursor),34 种纤维粥样瘤(fibroatheroma,FA)(AHA 分级 IV 和 V);和 11 种薄帽纤维粥样瘤(fibroatheroma with thin cap,TCFA,AHA 分级 IV)]。
纤维蛋白在 AIT 和 PIT 的内膜中通常不存在,在早期 FA 的核心中中度染色(2.6 +/- 0.3)。所有晚期 FA 和 TCFA 均显示核心内纤维蛋白,平均评分分别为 2.9 +/- 0.3 和 3.0 +/- 0.3。内膜血管丛计数随内膜纤维蛋白评分增加而增加(p < 0.0001);在 68%的纤维蛋白染色核心中,红细胞破裂的证据很少或没有。
坏死核心中的纤维蛋白与斑块内血管丛成正比,且早于红细胞,提示血管渗漏发生在斑块内出血之前。纤维蛋白可能在动脉粥样前体和动脉粥样硬化之间起桥梁作用。