Tsai Tzu-Hsien, Chua Sarah, Yang Cheng-Hsu, Hang Chi-Ling, Hsieh Yuan-Kai, Chen Yen-Hsun, Chai Han-Tan, Yeh Kuo-Ho, Yip Hon-Kan
Division of Cardiology, Chang Gung Memorial Hospital-Kaohsiung Medical Center, Chang Gung University College of Medicine, Kaohsiung, Taiwan.
Chang Gung Med J. 2007 Jul-Aug;30(4):313-20.
An elevated C-reactive protein (CRP) level plays a crucial role in cell biology of atherosclerosis and unstable plaque formation. However, direct evidence of CRP involvement in atherosclerotic plaque development and vulnerability is still limited. We hypothesized that CRP is present in the vulnerable plaques and that CRP staining intensity is stronger in vulnerable plaques compared to stable plaques.
Directional coronary atherectomy (DCA) was performed on 58 patients with stable angina (group 1) and 40 patients with unstable angina (group 2). White blood cell (WBC) counts were measured prior to DCA. Immunohistochemical staining (IHCS) was performed to localize CRP in the atheroma. Staining intensity in macrophages and extracellular tissue was graded as: 0, no staining; 1+, < 30%; 2+, 30%-60%; 3+, > 60%.
The IHCS demonstrated that CRP staining - 1+ intensity in macrophages and extracellular tissue were significantly higher in group 1 than in group 2 patients (all p values < 0.0001). However, IHCS demonstrated that CRP staining a 2+ intensity in macrophages and extracellular tissue were significantly higher in group 2 than in group 1 patients (all p values < 0.0001). By multiple analysis, only stable angina was independently associated with CRP staining : 1+ intensity in both macrophages and extracellular tissue (p < 0.0001), whereas unstable angina and WBC counts were independent predictors of CRP staining > or = 2+ intensity in both macrophages and extracellular tissue (p < 0.0001).
CRP was frequently found in atherosclerotic plaques of patients with unstable angina. This analytical finding suggests that CRP directly mediates an inflammatory process in the atherosclerotic plaque.
C反应蛋白(CRP)水平升高在动脉粥样硬化的细胞生物学和不稳定斑块形成中起关键作用。然而,CRP参与动脉粥样硬化斑块发展和易损性的直接证据仍然有限。我们推测CRP存在于易损斑块中,并且与稳定斑块相比,易损斑块中CRP染色强度更强。
对58例稳定型心绞痛患者(第1组)和40例不稳定型心绞痛患者(第2组)进行定向冠状动脉斑块旋切术(DCA)。在DCA术前测量白细胞(WBC)计数。进行免疫组织化学染色(IHCS)以在动脉粥样瘤中定位CRP。巨噬细胞和细胞外组织中的染色强度分级为:0,无染色;1 +,<30%;2 +,30% - 60%;3 +,>60%。
IHCS显示,第1组患者巨噬细胞和细胞外组织中CRP染色强度为1 +的比例显著高于第2组患者(所有p值<0.0001)。然而,IHCS显示,第2组患者巨噬细胞和细胞外组织中CRP染色强度为2 +的比例显著高于第1组患者(所有p值<0.0001)。通过多因素分析,仅稳定型心绞痛与巨噬细胞和细胞外组织中CRP染色强度为1 +独立相关(p < 0.0001),而不稳定型心绞痛和WBC计数是巨噬细胞和细胞外组织中CRP染色强度≥2 +的独立预测因素(p < 0.0001)。
在不稳定型心绞痛患者的动脉粥样硬化斑块中经常发现CRP。这一分析结果表明CRP直接介导动脉粥样硬化斑块中的炎症过程。