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Myocardial injury in critically Ill patients with community-acquired pneumonia a cohort study

Authors :
Esther Witteveen
Lonneke A. van Vught
Gerie J. Glas
Maria E. Koster-Brouwer
Janneke Horn
Arie J. Hoogendijk
Marcus J. Schultz
Marc J.M. Bonten
Luuk Wieske
Peter M. C. Klein Klouwenberg
Dirk W. Donker
David S. Y. Ong
Maryse A. Wiewel
Teus H. Kappen
Laura R. A. Schouten
Wilton A. van Klei
Lottie van Baal
Jos F. Frencken
Lieuwe D. J. Bos
Friso M. de Beer
Diana M. Verboom
Mischa A. Huson
Olaf L. Cremer
Marleen Straat
Tom van der Poll
Brendon P. Scicluna
Roosmarijn T. M. van Hooijdonk
Kirsten van de Groep
Intensive Care Medicine
ANS - Neuroinfection & -inflammation
Center of Experimental and Molecular Medicine
Infectious diseases
AII - Infectious diseases
Anesthesiology
Graduate School
ACS - Heart failure & arrhythmias
ACS - Diabetes & metabolism
APH - Quality of Care
Neurology
ANS - Amsterdam Neuroscience
APH - Health Behaviors & Chronic Diseases
Epidemiology and Data Science
ARD - Amsterdam Reproduction and Development
APH - Personalized Medicine
ACS - Pulmonary hypertension & thrombosis
ACS - Microcirculation
Source :
Annals of the American Thoracic Society, 16(5), 606-612. American Thoracic Society
Publication Year :
2019

Abstract

Rationale: 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. Objectives: Our aim was to determine the incidence of troponin release in patients with CAP and identify risk factors that 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 we used mixed-effects regression to model the daily rise and fall of troponin levels over time. Results: Of 200 eligible patients, 179 were included, yielding 792 observation days. A total of 152 (85%) patients developed raised troponin levels greater than 26 ng/L. Baseline factors independently associated with troponin release included coronary artery disease (176% increase; 95% confidence interval [CI], 11–589), smoking (248% increase; 95% CI, 33–809), and higher Acute Physiology and Chronic Health Evaluation IV score (2% increase; 95% CI, 0.8–3.3), whereas Staphylococcus aureus as a causative pathogen was protective (70% reduction; 95% CI, 18–89). Time-dependent risk factors independently associated with daily increase in troponin concentrations included reduced platelet count (2.3% increase; 95% CI, 0.6–4), tachycardia (1.5% increase; 95% CI, 0.1–2.9), hypotension (6.2% increase; 95% CI, 2.1–10.6), dobutamine use (44% increase; 95% CI, 12–85), prothrombin time (8.2% increase; 95% CI, 0.2–16.9), white cell count (1.7% increase; 95% CI, 0–3.5), and fever (22.7% increase; 95% CI, 0.1–49.6). Conclusions: Cardiac injury develops in a majority of patients with severe CAP. Myocardial oxygen supply–demand mismatch and activated inflammation/coagulation are associated with this injury.

Details

Language :
English
ISSN :
23256621
Database :
OpenAIRE
Journal :
Annals of the American Thoracic Society, 16(5), 606-612. American Thoracic Society
Accession number :
edsair.doi.dedup.....ee63315b9de98045e300c2cd5492c103