Blum Arnon, Costello Rene, Samsel Leigh, Zalos Gloria, McCoy Phil, Csako Gyorgy, Waclawiw Myron A, Cannon Richard O
Translational Medicine Branch, National Heart Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Isr Med Assoc J. 2009 Oct;11(10):602-5.
High sensitivity C-reactive protein, a marker of inflammation, has been proposed to stratify coronary artery disease risk and is lowered by HMG-CoA reductase (statin) therapy. However, the reproducibility of persistently elevated hs-CRP levels and association with other markers of inflammation in patients with stable CAD on aggressive statin therapy is unknown.
To determine the reproducibility of hs-CRP levels measured within 2 weeks in patients with documented CAD with stable symptoms and to identify associations with other markers of inflammation.
Levels of hs-CRP were measured twice within 14 days (7 +/- 4) in 23 patients (22 males and 1 female, average age 66 +/- 10 years) with stable CAD and hs-CRP > or = 2.0 mg/L but < or = 10 mg/L at visit 1. All patients had received statins for cholesterol management (low density lipoprotein-cholesterol 84 +/- 25 mg/dl) with no dose change for > 3 months. None had a history or evidence of malignancy, chronic infection or inflammation, or recent trauma. There was no change in medications between visits 1 and 2, and no patient reported a change in symptoms or general health during this interval. White blood cell count and pro- and anti-inflammatory cytokines were measured at both visits.
hs-CRP levels tended to be lower at visit 2 (median 2.4 mg/L, range 0.8-11 mg/L) than at visit 1 (median 3.3 mg/L, range 2.0-9.7; P = 0.1793). However, between the two visits hs-CRP levels decreased by more than 1.0 mg/L in 10 patients and increased by more than 1.0 mg/L in 4 patients. Changes in hs-CRP levels were unrelated to changes in levels of white blood cells (P = 0.4353). Of the cytokines tested, only the antiinflammatory cytokine interleukin-1 receptor antagonist and the pro-inflammatory cytokine interleukin-8 were above lower limits of detection, but there were no correlations between changes in these values and changes in hs-CRP (both P > 0.5).
In stable CAD patients on aggressive statin therapy, hs-CRP levels may fluctuate over brief periods in the absence of changes in health, cardiac symptom status and medications, and without corroboration with other measures of inflammation. Accordingly, elevated hs-CRP levels should be interpreted with caution in this setting.
高敏C反应蛋白作为一种炎症标志物，已被用于对冠状动脉疾病风险进行分层，且HMG-CoA还原酶（他汀类）治疗可使其降低。然而，对于接受强化他汀治疗的稳定型冠心病患者，高敏C反应蛋白水平持续升高的可重复性以及与其他炎症标志物的相关性尚不清楚。
确定症状稳定的确诊冠心病患者在2周内测量的高敏C反应蛋白水平的可重复性，并确定其与其他炎症标志物的相关性。
对23例（22例男性和1例女性，平均年龄66±10岁）稳定型冠心病且首次就诊时高敏C反应蛋白水平≥2.0mg/L但≤10mg/L的患者，在14天内（7±4天）测量两次高敏C反应蛋白水平。所有患者均接受他汀类药物治疗以控制胆固醇（低密度脂蛋白胆固醇84±25mg/dl），且3个月内未改变剂量。无人有恶性肿瘤、慢性感染或炎症病史或证据，也无近期外伤史。在第1次和第2次就诊期间未改变用药，且在此期间无患者报告症状或总体健康状况有变化。在两次就诊时均测量白细胞计数以及促炎和抗炎细胞因子。
第2次就诊时高敏C反应蛋白水平（中位数2.4mg/L，范围0.8 - 11mg/L）往往低于第1次就诊时（中位数3.3mg/L，范围2.0 - 9.7；P = 0.1793）。然而，在两次就诊期间，10例患者的高敏C反应蛋白水平下降超过1.0mg/L，4例患者的高敏C反应蛋白水平升高超过1.0mg/L。高敏C反应蛋白水平的变化与白细胞水平的变化无关（P = 0.4353）。在所检测的细胞因子中，只有抗炎细胞因子白细胞介素-1受体拮抗剂和促炎细胞因子白细胞介素-8高于检测下限，但这些值的变化与高敏C反应蛋白的变化之间无相关性（P均>0.5）。
在接受强化他汀治疗的稳定型冠心病患者中，在健康状况、心脏症状状态和用药无变化的情况下，高敏C反应蛋白水平可能在短时间内波动，且与其他炎症指标不相符。因此，在这种情况下，对高敏C反应蛋白水平升高的解读应谨慎。
