Burke Allen P, Tracy Russell P, Kolodgie Frank, Malcom Gray T, Zieske Arthur, Kutys Robert, Pestaner Joseph, Smialek John, Virmani Renu
Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC 20306-6000, USA.
Circulation. 2002 Apr 30;105(17):2019-23. doi: 10.1161/01.cir.0000015507.29953.38.
Elevations in serum C-reactive protein measured by high-sensitivity assay (hs-CRP) have been associated with unstable coronary syndromes. There have been no autopsy studies correlating hs-CRP to fatal coronary artery disease.
Postmortem sera from 302 autopsies of men and women without inflammatory conditions other than atherosclerosis were assayed for hs-CRP. There were 73 sudden deaths attributable to atherothrombi, 71 sudden coronary deaths with stable plaque, and 158 control cases (unnatural sudden deaths and noncardiac natural deaths without conditions known to elevate CRP). Atherothrombi were classified as plaque ruptures (n=55) and plaque erosion (n=18); plaque burden was estimated in each heart. Total cholesterol, high-density lipoprotein cholesterol, diabetes, smoking history, and body mass index were also determined. Immunohistochemical stains for CRP and numbers of thin cap atheromas per heart were quantitated in coronary deaths with hs-CRP in the highest and lowest quintiles. The median hs-CRP was 3.2 microg/mL in acute rupture, 2.9 microg/mL in plaque erosion, 2.5 microg/mL in stable plaque, and 1.4 microg/mL in controls. Mean log hs-CRP was higher in rupture (P<0.0001), erosion (P=0.005), and stable plaque (P=0.0003) versus controls. By multivariate analysis, atherothrombi (P=0.02), stable plaque (P=0.003), and plaque burden (P=0.03) were associated with log hs-CRP independent of age, sex, smoking, and body mass index. Mean staining intensity for CRP of macrophages and lipid core in plaques was significantly greater in cases with high hs-CRP than those with low CRP (P=0.0001), as were mean numbers of thin cap atheromas (P<0.0001).
hs-CRP is significantly elevated in patients dying suddenly with severe coronary artery disease, both with and without acute coronary thrombosis, and correlates with immunohistochemical staining intensity and numbers of thin cap atheroma.
通过高敏检测法（hs-CRP）测得的血清C反应蛋白升高与不稳定型冠状动脉综合征相关。尚无尸检研究将hs-CRP与致命性冠状动脉疾病相关联。
对302例除动脉粥样硬化外无炎症性疾病的男女尸检后的血清进行hs-CRP检测。有73例因动脉粥样硬化血栓形成导致的猝死，71例有稳定斑块的冠状动脉猝死，以及158例对照病例（非自然猝死和无已知可升高CRP情况的非心脏自然死亡）。动脉粥样硬化血栓分为斑块破裂（n = 55）和斑块侵蚀（n = 18）；估计每颗心脏的斑块负荷。还测定了总胆固醇、高密度脂蛋白胆固醇、糖尿病、吸烟史和体重指数。对hs-CRP处于最高和最低五分位数的冠状动脉死亡病例，对每颗心脏的CRP进行免疫组织化学染色并对薄帽纤维粥样斑块数量进行定量。急性破裂时hs-CRP的中位数为3.2μg/mL，斑块侵蚀时为2.9μg/mL，稳定斑块时为2.5μg/mL，对照为1.4μg/mL。与对照相比，破裂（P<0.0001）、侵蚀（P = 0.005）和稳定斑块（P = 0.0003）时的平均log hs-CRP更高。通过多变量分析，动脉粥样硬化血栓形成（P = 0.02）、稳定斑块（P = 0.003）和斑块负荷（P = 0.03）与log hs-CRP相关，独立于年龄、性别、吸烟和体重指数。hs-CRP高的病例中，斑块内巨噬细胞和脂质核心的CRP平均染色强度显著高于hs-CRP低的病例（P = 0.0001），薄帽纤维粥样斑块的平均数量也是如此（P<0.0001）。
在因严重冠状动脉疾病突然死亡的患者中，无论有无急性冠状动脉血栓形成，hs-CRP均显著升高，且与免疫组织化学染色强度和薄帽纤维粥样斑块数量相关。
