Boyle J J
Department of Pathology, Glasgow Royal Infirmary, U.K.
J Pathol. 1997 Jan;181(1):93-9. doi: 10.1002/(SICI)1096-9896(199701)181:1<93::AID-PATH696>3.0.CO;2-H.
Coronary plaque inflammation may promote plaque rupture and thrombosis. To test this hypothesis, 351 coronary plaques from 83 patients were formalin-fixed and stained with haematoxylin and eosin. There were six groups: (1) ruptured plaques; (2) intact plaques from recently infarcted hearts; (3) plaques from hearts with severe coronary atherosclerosis without identifiable thrombosis; (4) native explanted hearts with severe coronary atherosclerosis; (5) cardiac transplant atherosclerosis; and (6) fatalities unrelated to coronary atherosclerosis. Selected arteries were immunostained for leukocyte markers and serially sectioned to identify plaque rupture. There were infiltrates of CD68-positive macrophages and CD3- and CD8-positive T cells adjacent to all plaque ruptures. Labelling with HLA-DR and CD30 indicated inflammatory cell activation. Plaque rupture was strongly statistically associated with the severity and frequency of superficial plaque inflammation but not that of deep plaque inflammation. Although atherosclerotic inflammation has been identified adjacent to rupture, this is its first comparison with control plaques. These results support the concept that inflammation in the fibrous cap is particularly associated with plaque rupture.
冠状动脉斑块炎症可能会促进斑块破裂和血栓形成。为了验证这一假说，对来自83名患者的351个冠状动脉斑块进行福尔马林固定，并进行苏木精-伊红染色。分为六组：（1）破裂斑块；（2）近期梗死心脏的完整斑块；（3）有严重冠状动脉粥样硬化但无明显血栓形成的心脏斑块；（4）有严重冠状动脉粥样硬化的原位移植心脏；（5）心脏移植后的动脉粥样硬化；（6）与冠状动脉粥样硬化无关的死亡病例。对选定的动脉进行白细胞标志物免疫染色并连续切片以识别斑块破裂。所有斑块破裂处附近均有CD68阳性巨噬细胞以及CD3和CD8阳性T细胞浸润。HLA-DR和CD30标记显示炎症细胞活化。斑块破裂在统计学上与浅表斑块炎症的严重程度和频率密切相关，而与深部斑块炎症无关。虽然在破裂处附近已发现动脉粥样硬化炎症，但这是首次将其与对照斑块进行比较。这些结果支持了纤维帽中的炎症尤其与斑块破裂相关的概念。
