• Jian-Jun Li, Hong Jiang, Cong-Xin Huang, Chun-Hong Fang, Qi-Zhu Tang, Hao Xia, Jun Liu, and Geng-Shan Li.
• Department of Cardiology, Renmin Hospital, Wuhan University School of Medicine, People's Republic of China. lijnjn@263.net
• Angiology. 2002 May 1; 53 (3): 265-72.

AbstractC-reactive protein (CRP) is a sensitive marker of inflammation, and elevated levels have been associated with future risk of cardiovascular events. To explore the role and relationship of CRP and coronary stenosis in the development of unstable angina (UA), plasma levels of CRP were determined on admission in 45 patients with UA, and in 42 patients with stable angina (SA) using high-sensitivity ELISA. Coronary angiography was performed in all patients with coronary heart disease (CHD), and severity of coronary stenosis was evaluated by a quantitative analysis. Lipid measurement was performed using automatic biochemical analyzer. Data available from patients with CHD were compared with those of 41 control subjects. The results showed that plasma levels of CRP are significantly higher in patients with UA than those in patients with SA and control subjects (5.1 +/- 1.4 mg/L vs 1.7 +/- 0.4 mg/L and 1.3 +/- 0.2 mg/L, p<0.01, respectively) with no difference between the latter two groups (p>0.05); the total incidence of clinical events during in-hospital follow-up was higher in the group A (p<0.01); the scores of coronary stenosis are significantly higher in patients with SA than those in patients with UA (4.9 +/- 2.1 vs 3.4 +/- 1.4, p<0.05); there is no correlation between plasma levels of CRP and serum total cholesterol (TC) as well as high-density lipoprotein cholesterol (HDL-C) in both groups (p>0.05 respectively); there was no correlation between plasma levels of CRP and severity of coronary stenosis was found in patients with UA (p>0.05) but a significant positive association in patients with SA (p<0.001); and the patients with persistent, severe, treatment-unresponsive UA had significantly higher CRP levels as well as incidence of clinical events than patients with treatment-responsive UA (7.4 +/- 1.8 mg/L vs 2.6 +/- 1.3 mg/L, p<0.01; 0 vs 22.2%, p<0.05). The present data suggested that inflammation may play an important role in the pathogenesis of UA, and the plasma levels of CRP might have a higher prognostic value than the severity of coronary stenosis correlated with the clinical outcome of instability despite of lipid profile status.

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