The Relationship Between Cardiac Troponin in People Hospitalised for Exacerbation of COPD and Major Adverse Cardiac Events (MACE) and COPD Readmissions

Abstract

Background

No single biomarker currently risk stratifies chronic obstructive pulmonary disease (COPD) patients at the time of an exacerbation, though previous studies have suggested that patients with elevated troponin at exacerbation have worse outcomes. This study evaluated the relationship between peak cardiac troponin and subsequent major adverse cardiac events (MACE) including all-cause mortality and COPD hospital readmission, among patients admitted with COPD exacerbation.

Methods

Data from five cross-regional hospitals in England were analysed using the National Institute of Health Research Health Informatics Collaborative (NIHR-HIC) acute coronary syndrome database (2008–2017). People hospitalised with a COPD exacerbation were included, and peak troponin levels were standardised relative to the 99th percentile (upper limit of normal). We used Cox Proportional Hazard models adjusting for age, sex, laboratory results and clinical risk factors, and implemented logarithmic transformation (base-10 logarithm). The primary outcome was risk of MACE within 90 days from peak troponin measurement. Secondary outcome was risk of COPD readmission within 90 days from peak troponin measurement.

Results

There were 2487 patients included. Of these, 377 (15.2%) patients had a MACE event and 203 (8.2%) were readmitted within 90 days from peak troponin measurement. A total of 1107 (44.5%) patients had an elevated troponin level. Of 1107 patients with elevated troponin at exacerbation, 256 (22.8%) had a MACE event and 101 (9.0%) a COPD readmission within 90 days from peak troponin measurement. Patients with troponin above the upper limit of normal had a higher risk of MACE (adjusted HR 2.20, 95% CI 1.75–2.77) and COPD hospital readmission (adjusted HR 1.37, 95% CI 1.02–1.83) when compared with patients without elevated troponin.

Conclusion

An elevated troponin level at the time of COPD exacerbation may be a useful tool for predicting MACE in COPD patients. The relationship between degree of troponin elevation and risk of future events is complex and requires further investigation.

Keywords:

• COPD
• CVD
• exacerbation

Ethics Approval

This study was approved by the London-South East Research Ethics Committee (REC reference: 16/HRA/3327). Consent was waived due to the retrospective nature of the study, all data were anonymized and patient confidentiality maintained.

Acknowledgments

The abstract of this paper was presented at the International Conference of the American Thoracic Society (ATS) 2023 as an abstract presentation with interim findings. The poster’s abstract was published in “Poster Abstracts” in American Journal of Respiratory and Critical Care Medicine, Volume 207 Supplement S Meeting Abstract A6419, DOI:10.1164/ajrccm-conference.2023.207.1_MeetingAbstracts.A6419.

Disclosure

Dr Richard Lee is funded by the Royal Marsden NIHR BRC and Royal Marsden Cancer Charity. Dr Lee’s institution receives compensation for time spent in a secondment role for the NHS England Targeted lung health check programme, and as a national specialty lead for the National Institute of Health and Care Research. He has received research funding from CRUK, Innovate UK (co-funded by GE Healthcare, Roche and Optellum), SBRI (co-applicant in grants with QURE.AI), RM Partners Care Alliance and NIHR (co-applicant in grants with Optellum). He has received honoraria from CRUK. Dr Anoop D. Shah is supported by grants from NIHR (AI_AWARD01864 and COV-LT-0009), UKRI (Horizon Europe Guarantee for DataTools4Heart) and British Heart Foundation Accelerator Award (AA/18/6/24223). Professor Nick Curzen reports grants from Backmann Coulter, during the conduct of the study; grants and/or personal fees from Haemonetics, Boston Scientific, Heartflow, and Abbott, outside the submitted work. Professor Ajay Shah reports personal fees from Forcefield Therapeutics and CYTE, outside the submitted work. Professor Jamil Mayet is supported by a BHF Consultant Research Award (FS/CRA/22/23036) and the BHF Imperial Centre for Research Excellence (RE/18/4/34215). The authors report no other conflicts of interest in this work.

Additional information

Funding

The research was supported by the National Institute for Health Research (NIHR) Biomedical Research Centres at Imperial, King’s, Oxford, UCLH, Royal Marsden and ICR, Leeds, Manchester, Southampton, Leicester, Bristol, and Guys & St Thomas’. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.