Yip Hon-Kan, Wu Chiung-Jen, Chang Hsueh-Wen, Yang Cheng-Hsu, Yeh Kuo-Ho, Chua Sarah, Fu Morgan
Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung, 123, Ta Pei Rd, Niao Sung Hsiang, Kaohsiung Hsien, 83301, Taiwan, ROC.
Chest. 2004 Nov;126(5):1417-22. doi: 10.1378/chest.126.5.1417.
C-reactive protein (CRP), which has been suggested to directly enhance inflammation in plaques, is rapidly synthesized and secreted in the liver 6 h after an acute inflammatory stimulus. Therefore, serum levels of CRP within 6 h after the onset of acute myocardial infarction (AMI) merely reflect a chronic and persistent inflammatory process and are not due to acute myocardial damage. We hypothesized that the serum CRP level, which would abnormally elevate thereafter, is followed by a plaque rupture in the clinical setting of AMI.
CRP was prospectively measured by high-sensitivity CRP assay (hs-CRP) in 157 consecutive patients (106 patients within 6 h, and 51 patients >/= 6 h but < 12 h after the onset of AMI) with ST-segment elevation AMI undergoing primary percutaneous coronary intervention (PCI). Serum levels of hs-CRP were also measured in 30 patients with stable angina undergoing elective PCI and in 30 healthy control subjects. The serum level of hs-CRP was significantly higher in patients with an onset of AMI < 6 h than in patients with angina pectoris (2.7 +/- 2.3 mg/L vs 1.4 +/- 0.7 mg/L, p < 0.0001 [mean +/- SD]) and in healthy subjects (2.7 +/- 2.3 mg/L vs 1.0 +/- 0.6 mg/L, p < 0.0001). There were no significant differences in serum levels of hs-CRP in patients with an onset of AMI </= 3 h than in those patients with an onset of AMI > 3 h but < 6 h (2.7 +/- 2.5 mg/L vs 2.7 +/- 2.2 mg/L, p = 0.87). However, the serum level of hs-CRP was significantly higher in patients with an onset >/= 6 h than in patients with an onset < 6 h (14.1 +/- 16.5 mg/L vs 2.7 +/- 2.3 mg/L, p < 0.0001).
Serum levels of hs-CRP were significantly higher in patients with an onset of AMI < 6 h than in healthy subjects and in patients with angina pectoris undergoing PCI. The inflammatory process has been proved as one of the mechanisms causing plaque rupture. Elevated serum hs-CRP levels in patients with AMI < 6 h may portend vulnerable plaque rupture.
C反应蛋白（CRP）被认为可直接增强斑块内的炎症反应，在急性炎症刺激后6小时在肝脏中迅速合成并分泌。因此，急性心肌梗死（AMI）发作后6小时内的血清CRP水平仅反映慢性持续性炎症过程，而非急性心肌损伤所致。我们假设，在AMI临床情况下，随后异常升高的血清CRP水平会伴随斑块破裂。
采用高敏CRP检测法（hs-CRP）对157例接受直接经皮冠状动脉介入治疗（PCI）的ST段抬高型AMI连续患者（106例发病6小时内，51例发病≥6小时但<12小时）进行前瞻性CRP检测。还对30例接受择期PCI的稳定型心绞痛患者和30例健康对照者检测了hs-CRP血清水平。AMI发病<6小时的患者hs-CRP血清水平显著高于心绞痛患者（2.7±2.3mg/L对1.4±0.7mg/L，p<0.0001[均值±标准差]）和健康受试者（2.7±2.3mg/L对1.0±0.6mg/L，p<0.0001）。AMI发病≤3小时的患者与发病>3小时但<6小时的患者hs-CRP血清水平无显著差异（2.7±2.5mg/L对2.7±2.2mg/L，p = 0.87）。然而，发病≥6小时的患者hs-CRP血清水平显著高于发病<6小时的患者（14.1±16.5mg/L对2.7±2.3mg/L，p<0.0001）。
AMI发病<6小时的患者hs-CRP血清水平显著高于健康受试者和接受PCI的心绞痛患者。炎症过程已被证明是导致斑块破裂的机制之一。AMI发病<6小时患者血清hs-CRP水平升高可能预示易损斑块破裂。
