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S100 Relationship of cardiac biomarkers in COPD at stable state and exacerbation

thoraxjnl · 2025-11-02 · canonical JSON source

10 visible annotations · policy: published · automated confidence ≥ 75.00%

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Introduction Cardiac biomarkers are frequently raised in patients with COPD. Our aim was to understand the relationship between troponin and BNP at both stable state COPD and during an exacerbation.Methods Patients with COPD were prospectively recruited from 14 GP practices as part of the STARR2 study. 1 Blood sampling was obtained at stable state, exacerbation (day 0), and 14 and 30 days later. Troponin and BNP levels were measured at each time point using commercial ELISA kits (R&D systems, Troponin LLD 125pg/mL and R&D systems, BNP LDD 312pg/ml).Spearman’s rank test was undertaken to assess the relationship between troponin and BNP at stable state, and the relationship between troponin and BNP rise for each exacerbation.Results 65 patients were included in the study, 66% were male, median age was 72 (IQR 66.5–76.5) years. 13 patients (20%) had IHD, 5 (7.6%) known atrial fibrillation and 3 (4.6%) a diagnosis of heart failure.A significant positive correlation was found between troponin and BNP at stable state (r=0.53; p<0.001) but no correlation was observed between peak troponin rise and peak BNP rise within 30 days of moderate COPD exacerbation (r=0.071; p=0.57). We identified 4 clusters of cardiac biomarker changes during exacerbation: 10 patients (15.4%) had a significant rise in both troponin and BNP, 11 patients (16.9%) had a significant rise in troponin only; 15 patients (23.1%) had a significant rise in BNP only and 29 patients (44.6%) had neither a troponin nor BNP rise.Conclusion To our knowledge this is the first study investigating the relationship between different cardiac biomarkers in COPD at stable state and exacerbation. BNP and troponin levels exhibited a similar pattern of baseline cardiac stress at stable state but no relationship was observed between troponin and BNP rise during moderate exacerbation. These results suggest that different endotypes of cardiac injury may exist at exacerbation. Further work is needed to understand if there are different pathophysiological mechanisms accounting for different clusters of cardiac injury at exacerbation.Reference Ramakrishnan S, et al. Blood eosinophil-guided oral prednisolone for COPD exacerbations in primary care in the UK (STARR2). Lancet Respir Med. 2024.