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Myocardial injury in critically ill patients with community-acquired pneumonia

View ORCID ProfileJos. F. Frencken, Lottie van Baal, Teus H. Kappen, Dirk W. Donker, Janneke Horn, Tom van der Poll, Wilton A. van Klei, Marc J.M. Bonten, Olaf L. Cremer, on behalf of the MARS consortium
doi: https://doi.org/10.1101/155747
Jos. F. Frencken
1Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands
2Department of Intensive Care Medicine, University Medical Center Utrecht, Utrecht, the Netherlands
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  • ORCID record for Jos. F. Frencken
Lottie van Baal
2Department of Intensive Care Medicine, University Medical Center Utrecht, Utrecht, the Netherlands
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Teus H. Kappen
3Department of Anesthesiology, University Medical Center Utrecht, Utrecht, the Netherlands
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Dirk W. Donker
2Department of Intensive Care Medicine, University Medical Center Utrecht, Utrecht, the Netherlands
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Janneke Horn
4Department of Intensive Care, Academic Medical Center, Amsterdam, the Netherlands
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Tom van der Poll
5Center for Experimental and Molecular Medicine, Academic Medical Center, Amsterdam, the Netherlands
6Division of Infectious Diseases, Academic Medical Center, Amsterdam, the Netherlands
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Wilton A. van Klei
3Department of Anesthesiology, University Medical Center Utrecht, Utrecht, the Netherlands
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Marc J.M. Bonten
1Julius Center for Health Sciences and Primary Care, University Medical Center Utrecht, Utrecht, the Netherlands
7Department of Medical Microbiology, University Medical Center Utrecht, Utrecht, the Netherlands
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Olaf L. Cremer
2Department of Intensive Care Medicine, University Medical Center Utrecht, Utrecht, the Netherlands
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Abstract

Background Myocardial injury, as reflected by elevated cardiac troponin levels in plasma, is common in patients with community-acquired pneumonia (CAP), but its temporal dynamics and etiology remain unknown. Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors which may point to underlying etiologic mechanisms.

Methods We included consecutive patients admitted with severe CAP to two intensive care units in the Netherlands between 2011 and 2015. High-sensitivity cardiac troponin I was measured daily during the first week. We used multivariable linear regression to identify variables associated with troponin release on admission, and mixed-effects regression to model the daily rise and fall of troponin levels over time.

Results Among 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels >26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (160% increase, 95% CI 7–529), smoking (304% increase, 95% CI 59-924), and higher APACHE IV score (2% increase, 95% CI 0.7-3.3), whereas Staphylococcus aureus as a causative pathogen was protective (67% reduction, 95% CI 9-88). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (1.7% increase, 95% CI 0.1-3.4), tachycardia (1.6% increase, 95% CI 0.3-3), hypotension (5.1% increase, 95% CI 1-9.4) and dobutamine use (38.4% increase 95% CI 8.8-76).

Conclusions Cardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply-demand mismatch and activated coagulation are potential causes of this injury.

Copyright 
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license.
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Posted June 28, 2017.
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Myocardial injury in critically ill patients with community-acquired pneumonia
Jos. F. Frencken, Lottie van Baal, Teus H. Kappen, Dirk W. Donker, Janneke Horn, Tom van der Poll, Wilton A. van Klei, Marc J.M. Bonten, Olaf L. Cremer, on behalf of the MARS consortium
bioRxiv 155747; doi: https://doi.org/10.1101/155747
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Myocardial injury in critically ill patients with community-acquired pneumonia
Jos. F. Frencken, Lottie van Baal, Teus H. Kappen, Dirk W. Donker, Janneke Horn, Tom van der Poll, Wilton A. van Klei, Marc J.M. Bonten, Olaf L. Cremer, on behalf of the MARS consortium
bioRxiv 155747; doi: https://doi.org/10.1101/155747

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