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Systemic inflammation induced by exacerbation of COPD or pneumonia in patients with COPD induces cardiac troponin elevation
BMJ Open Respiratory Research ( IF 3.6 ) Pub Date : 2021-08-01 , DOI: 10.1136/bmjresp-2021-000997
Vidar Søyseth 1, 2 , Natalia Kononova 3, 4 , Anke Neukamm 5 , Nils Henrik Holmedahl 6 , Tor-Arne Hagve 7 , Torbjorn Omland 2, 8 , Gunnar Einvik 3, 4
Affiliation  

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. Data are available on reasonable request.

中文翻译:

慢性阻塞性肺病患者因慢性阻塞性肺病加重或肺炎引起的全身炎症诱导心肌肌钙蛋白升高

背景肌钙蛋白是心肌损伤的生物标志物。在慢性阻塞性肺病 (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,我们研究了与稳定期 COPD 相比,AECOPD 中的肌钙蛋白是否增加。方法 我们纳入了来自阿克斯胡斯大学医院服务区的 320 名稳定状态的 COPD 患者和 63 名随机个体。所有参与者均≥40 岁(平均 65·1 岁,标准差 7·6),176 人(46%)为女性。高敏心肌肌钙蛋白 T (hs-cTnT) 的几何平均值为 6·9 ng/L (geometric-SD 2·6)。随后的 5 年对他们的入院情况进行了跟踪。结果 在 5 年的随访中,我们注意到 474 例住院:总共,分别有 150 和 80 人因 AECOPD 或肺炎入院。入院时cTnT与AECOPD和肺炎稳定状态的几何平均比(GSE)分别为1·27(GSE=1.11,p=0·023)和1·28(GSE=1.14,p=0·054) ), 分别。在将住院时的血白细胞计数和 C 反应蛋白包括在内后,这些比率减至零。然而,我们估计 AECOPD 和肺炎对入院时 hs-cTnT 和稳定状态之间的比率的间接影响为 1·16(p=0·022)和 1·22(p=0·008),占 91%( 95% CI 82% 至 100%) 和 95% (95% CI 83% 至 100%) 分别。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介导的。可根据合理要求提供数据。
更新日期:2021-08-27
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