Abstract
Chronic obstructive pulmonary disease (COPD) is a leading cause of death with a considerable part of the population dying from cardiovascular diseases. High-sensitivity troponin I (hs-TnI) might help to better identify COPD patients at high risk of mortality. We aimed to study the predictive value of hs-TnI for all-cause mortality beyond established COPD assessments, and after consideration of relevant cardiovascular risk factors and prevalent cardiovascular diseases, in a broad population with stable COPD.
Circulating hs-TnI concentrations together with a wide range of respiratory and cardiovascular markers were evaluated in 2085 patients with stable COPD across all severity stages enrolled in the multicentre COSYCONET cohort study. The primary outcome was all-cause mortality over 3 years of follow-up.
Hs-TnI was detectable in 2020 (96.9%) patients. The median hs-TnI concentration was 3.8 ng·L−1 (interquartile range 2.5–6.6 ng·L−1), with levels above the 99th percentile reference limit of 27 ng·L−1 observed in 1.8% of patients. In Cox regression analyses including adjustments for airflow limitation, dyspnoea grade, exercise capacity and history of severe exacerbations, as well as traditional cardiovascular risk factors, estimated glomerular filtration rate, ankle–brachial index, N-terminal pro-brain natriuretic peptides and prevalent cardiovascular diseases, hs-TnI was a significant predictor for all-cause mortality, both as a continuous variable (hazard ratio (HR) for log hs-TnI 1.28, 95% CI 1.01–1.62) and categorised according to the cut-off of 6 ng·L−1 (HR 1.63, 95% CI 1.10–2.42).
In patients with stable COPD, hs-TnI is a strong predictor of all-cause mortality beyond established COPD mortality predictors, and independent of a broad range of cardiovascular risk factors and prevalent cardiovascular diseases. Hs-TnI concentrations well below the upper reference limit provide further prognostic value for all patients with COPD when added to established risk assessments.
Abstract
High-sensitivity troponin I is a strong predictor of all-cause mortality in patients with stable COPD independent from established mortality predictors of COPD and irrespective of their cardiovascular risk profile http://bit.ly/352ZtDw
Footnotes
This article has supplementary material available from erj.ersjournals.com
The study is registered at clinicaltrials.gov with identifier number NCT01245933.
Support statement: This work was supported by the German Federal Ministry of Education and Research (BMBF) Competence Network Asthma and COPD (ASCONET) and performed in collaboration with the German Centre for Lung Research (DZL). The project is funded by the BMBF with grant number 01 GI 0881, and is supported by unrestricted grants from AstraZeneca GmbH, Bayer Schering Pharma AG, Boehringer Ingelheim Pharma GmbH & Co. KG, Chiesi GmbH, GlaxoSmithKline, Grifols Deutschland GmbH, MSD Sharp & Dohme GmbH, Mundipharma GmbH, Novartis Deutschland GmbH, Pfizer Pharma GmbH, Takeda Pharma Vertrieb GmbH & Co. KG for patient investigations and laboratory measurements. The present analysis is also supported by the German Center for Cardiovascular Research (DZHK) under grant number 81Z1710101. The funding body had no involvement in the design of the study or the collection, analysis or interpretation of the data. Funding information for this article has been deposited with the Crossref Funder Registry.
Conflict of interest: B. Waschki has nothing to disclose.
Conflict of interest: P. Alter reports grants from German Federal Ministry of Education and Research (BMBF) Competence Network Asthma and COPD (ASCONET), AstraZeneca GmbH, GlaxoSmithKline, Grifols Deutschland GmbH, MSD Sharp and Dohme GmbH, Pfizer Pharma GmbH and Takeda Pharma Vertrieb GmbH & Co. KG, grants and non-financial support from Bayer Schering Pharma AG and Chiesi GmbH, grants, personal fees and non-financial support from Boehringer Ingelheim Pharma GmbH & Co. KG and Novartis Deutschland GmbH, grants and personal fees from Mundipharma GmbH, outside the submitted work.
Conflict of interest: T. Zeller has nothing to disclose.
Conflict of interest: C. Magnussen has nothing to disclose.
Conflict of interest: J.T. Neumann reports personal fees from Abbott Diagnostics and Siemens, outside the submitted work.
Conflict of interest: R. Twerenbold reports grants from Swiss National Science Foundation (grant number P300PB_167803), Swiss Heart Foundation, Swiss Society of Cardiology and Cardiovascular Research Foundation Basel, personal fees from Abbott Diagnostics, Amgen, Roche Diagnostics, Siemens, Singulex and Brahms, outside the submitted work.
Conflict of interest: C. Sinning has nothing to disclose.
Conflict of interest: C. Herr has nothing to disclose.
Conflict of interest: K. Kahnert has nothing to disclose
Conflict of interest: S. Fähndrich has nothing to disclose.
Conflict of interest: S. Blankenberg reports personal fees from Abbott Diagnostics, Siemens, Thermo Fisher and Singulex outside the submitted work.
Conflict of interest: K.F. Rabe has nothing to disclose.
Conflict of interest: T. Welte reports personal fees for lectures and advisory board work from AstraZeneca, Boehringer, Berlin Chemie, Chiesi, GSK and Novartis, grants from AstraZeneca and Novartis, outside the submitted work.
Conflict of interest: R.A. Jörres has nothing to disclose.
Conflict of interest: C.F. Vogelmeier reports grants and personal fees from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, Grifols and Novartis, personal fees from CSL Behring, Chiesi, Menarini, Mundipharma, Teva and Cipla, grants from Bayer-Schering, MSD and Pfizer, outside the submitted work.
Conflict of interest: R. Bals reports grants and personal fees from AstraZeneca, Boehringer Ingelheim and Novartis, personal fees from GlaxoSmithKline, Grifols and CSL Behring, grants from German Federal Ministry of Education and Research (BMBF) Competence Network Asthma and COPD (ASCONET), Sander Stiftung, Schwiete Stiftung, Krebshilfe and Mukoviszidose eV, outside the submitted work.
Conflict of interest: H. Watz reports personal fees from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline, BerlinChemie, Chiesi, Novartis and Roche, outside the submitted work.
- Received July 3, 2019.
- Accepted November 11, 2019.
- Copyright ©ERS 2020
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