COPD 患者因 COPD 恶化或肺炎引起的全身炎症会导致心肌肌钙蛋白升高。
Systemic inflammation induced by exacerbation of COPD or pneumonia in patients with COPD induces cardiac troponin elevation.
机构信息
Medical Division, Akershus University Hospital, Lorenskog, Norway
Campus Ahus, University of Oslo Faculty of Medicine, Lorenskog, Norway.
出版信息
BMJ Open Respir Res. 2021 Aug;8(1). doi: 10.1136/bmjresp-2021-000997.
BACKGROUND
Troponin is a biomarker of myocardial injury. In chronic obstructive pulmonary disease (COPD), troponin is an important determinant of mortality after acute exacerbation. Whether acute exacerbation of COPD (AECOPD) causes troponin elevation is not known. Here, we investigated whether troponin is increased in AECOPD compared to stable COPD.
METHODS
We included 320 patients with COPD in the stable state and 63 random individuals from Akershus University hospital's catchment area. All participants were ≥40 years old (mean 65·1 years, SD 7·6) and 176 (46%) were females. The geometric mean of high-sensitivity cardiac troponin T (hs-cTnT) was 6·9 ng/L (geometric-SD 2·6). They were followed regarding hospital admission for the subsequent 5 years.
RESULTS
During the 5-year follow-up, we noted 474 hospitalisations: Totally, 150 and 80 admissions were due to AECOPD or pneumonia, respectively. The geometric mean ratio with geometric SE GSE) between cTnT at admission and stable state in AECOPD and pneumonia was 1·27 (GSE=1.11, p=0·023) and 1·28 (GSE=1.14, p=0·054), respectively. After inclusion of blood leucocyte count and C reactive protein at hospitalisation, these ratios attenuated to zero. However, we estimated an indirect of AECOPD and pneumonia on the ratio between hs-cTnT at admission and the stable state to 1·16 (p=0·022) and 1·22 (p=0·008), representing 91% (95% CI 82% to 100%) and 95% (95% CI 83% to 100%) of the total effects, respectively.
CONCLUSION
AECOPD and pneumonia in patients with COPD is associated with higher cTnT levels. This association appears to be mediated by systemic inflammation.
背景
肌钙蛋白是心肌损伤的生物标志物。在慢性阻塞性肺疾病（COPD）中，肌钙蛋白是急性加重后死亡率的重要决定因素。COPD 急性加重（AECOPD）是否会导致肌钙蛋白升高尚不清楚。在这里，我们研究了 AECOPD 是否比稳定的 COPD 引起肌钙蛋白升高。
方法
我们纳入了 320 名稳定状态的 COPD 患者和阿克什胡斯大学医院辖区的 63 名随机个体。所有参与者年龄均≥40 岁（平均 65.1 岁，标准差 7.6），其中 176 名（46%）为女性。高敏心肌肌钙蛋白 T（hs-cTnT）的几何均数为 6.9ng/L（几何标准差 2.6）。随后对他们进行了后续 5 年的住院观察。
结果
在 5 年的随访期间，我们注意到了 474 次住院：总共，150 次和 80 次住院分别是由于 AECOPD 或肺炎引起的。AECOPD 和肺炎患者入院时与稳定状态时的 cTnT 之间的几何均值比（GSE）为 1.27（GSE=1.11，p=0.023）和 1.28（GSE=1.14，p=0.054）。在纳入住院时的白细胞计数和 C 反应蛋白后，这些比值衰减到零。然而，我们估计 AECOPD 和肺炎对入院时和稳定状态时 hs-cTnT 比值的间接影响为 1.16（p=0.022）和 1.22（p=0.008），分别代表 91%（95%CI 82%至 100%）和 95%（95%CI 83%至 100%）的总效应。
结论
COPD 患者的 AECOPD 和肺炎与较高的 cTnT 水平相关。这种关联似乎是由全身炎症引起的。
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