TY - JOUR
T1 - Myocardial injury in critically Ill patients with community-acquired pneumonia a cohort study
AU - Frencken, Jos F.
AU - van Baal, Lottie
AU - Kappen, Teus H.
AU - Donker, Dirk W.
AU - Horn, Janneke
AU - van der Poll, Tom
AU - van Klei, Wilton A.
AU - Bonten, Marc J.M.
AU - Cremer, Olaf L.
AU - on behalf of the MARS consortium
N1 - Funding Information:
*A complete list of members of the MARS Consortium can be found before the REFERENCES. Supported by the Center for Translational Molecular Medicine (www.ctmm.nl), MARS project (grant 04I-201). Author Contributions: J.F.F., L.v.B., T.H.K., D.W.D., J.H., T.v.d.P., W.A.v.K., M.J.M.B., and O.L.C.: substantially contributed to the conception and design of the study; J.F.F. and L.v.B.: acquired the data; J.F.F. and L.v.B.: had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis; J.F.F., L.v.B., T.H.K., W.A.v.K., M.J.M.B., and O.L.C.: were involved in the interpretation of the data; and J.F.F. and O.L.C.: drafted the manuscript. All authors revised the manuscript critically for important intellectual content, and all authors gave final approval of the version to be submitted.
Publisher Copyright:
Copyright © 2019 by the American Thoracic Society
PY - 2019/5/1
Y1 - 2019/5/1
N2 - 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.
AB - 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.
KW - Community-acquired pneumonia
KW - Etiology
KW - Myocardial injury
KW - Sepsis
KW - n/a OA procedure
UR - http://www.scopus.com/inward/record.url?scp=85065030580&partnerID=8YFLogxK
U2 - 10.1513/AnnalsATS.201804-286OC
DO - 10.1513/AnnalsATS.201804-286OC
M3 - Article
C2 - 30521759
AN - SCOPUS:85065030580
SN - 2329-6933
VL - 16
SP - 606
EP - 612
JO - Annals of the American Thoracic Society
JF - Annals of the American Thoracic Society
IS - 5
ER -
