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(Chest. 2004;126:1417-1422.)
© 2004 American College of Chest Physicians

Levels and Values of Serum High-Sensitivity C-Reactive Protein Within 6 Hours After the Onset of Acute Myocardial Infarction*

Hon-Kan Yip, MD; Chiung-Jen Wu, MD; Hsueh-Wen Chang, PhD; Cheng-Hsu Yang, MD; Kuo-Ho Yeh, MD; Sarah Chua, MD, FCCP and Morgan Fu, MD

* From the Division of Cardiology, Chang Gung Memorial Hospital, Kaohsiung, Department of Biological Sciences, National Sun Yat-Sen University, Kaohsiung, Taiwan, ROC.

Correspondence to: Morgan Fu, MD, Division of Cardiology, Department of Internal Medicine, Chang Gung Memorial Hospital, Kaohsiung, 123, Ta Pei Rd, Niao Sung Hsiang, Kaohsiung Hsien, 83301, Taiwan, ROC; e-mail: tang{at}adm.cgmh.org.tw

Background: 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.

Methods and results: 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).

Conclusions: 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.

Key Words: acute myocardial infarction • high-sensitivity C-reactive protein




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