The influence of heart failure co-morbidity on high-sensitivity troponin T levels in COPD exacerbation in a prospective cohort study: data from the Akershus cardiac examination (ACE) 2 study

Abstract

Context: Troponin (hs-TnT) levels predict mortality after acute exacerbation of COPD (AECOPD). Whether this is independent of heart failure (HF) is not established.

Material and methods: Prospectively included AECOPD patients adjudicated for acute HF categorized into three groups: (A) AECOPD, but acute HF the primary cause for hospitalization; (B) AECOPD the primary cause, but co-existing myocardial dysfunction and (C) AECOPD without myocardial dysfunction.

Results: About 103 AECOPD patients; 18% A, 27% B and 54% C. Hs-TnT level differed between the groups: (ng/l, median) A: 41, B: 25 and C: 15, p = 0.03 for A versus B and p = 0.005 for B versus C. During a median 826 days, 47% died. In Cox analysis, hs-TnT levels remained associated with mortality (hazard ratio per 10 ng/l 1.3, p < 0.0001).

Conclusion: hs-TnT levels are influenced by myocardial dysfunction/HF in AECOPD, but provide independent prognostic information. The prognostic merit of hs-TnT cannot be attributed to HF alone.

• COPD
• epidemiology
• heart failure
• troponin

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Corrigendum

Acknowledgements

We would like to acknowledge the contribution by Annika Lorentzen, BSc, Vigdis Bakkelund, BSc and Marit Jørgensen, BSc, to the blood sampling and Susann C. Brunell, BSc, Division of Diagnostics and Technology, Akershus University Hospital to hs-TnT and NT-proBNP analyses.

Declaration of interest

Roche Diagnostics supported the study by providing reagents at a reduced price to Akershus University Hospital (TAH). T.O. has received speaker’s honoraria from Abbott Diagnostics, Siemens Healthcare Diagnostics and Roche Diagnostics; research grant support from Abbott Diagnostics and Roche Diagnostics through Akershus University Hospital and a grant from the Norwegian Research Council to perform the ACE 2 Study. The other authors have no disclosures relating to this work.

Supplementary materials available on line

Supplementary Tables S1 and S2