TY - JOUR
T1 - Myocardial injury in critically Ill patients with community-acquired pneumonia a cohort study
AU - on behalf of the MARS consortium
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 - de Beer, Friso M.
AU - Bos, Lieuwe D. J.
AU - Glas, Gerie J.
AU - van Hooijdonk, Roosmarijn T. M.
AU - Schouten, Laura R. A.
AU - Straat, Marleen
AU - Witteveen, Esther
AU - Wieske, Luuk
AU - van Vught, Lonneke A.
AU - Wiewel, Maryse
AU - Hoogendijk, Arie J.
AU - Huson, Mischa A.
AU - Scicluna, Brendon
AU - Schultz, Marcus J.
AU - Ong, David S. Y.
AU - Klein Klouwenberg, Peter M. C.
AU - van de Groep, Kirsten
AU - Verboom, Diana
AU - Koster-Brouwer, Maria E.
PY - 2019
Y1 - 2019
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.
UR - https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=85065030580&origin=inward
UR - https://www.ncbi.nlm.nih.gov/pubmed/30521759
U2 - https://doi.org/10.1513/AnnalsATS.201804-286OC
DO - https://doi.org/10.1513/AnnalsATS.201804-286OC
M3 - Article
C2 - 30521759
SN - 2325-6621
VL - 16
SP - 606
EP - 612
JO - Annals of the American Thoracic Society
JF - Annals of the American Thoracic Society
IS - 5
ER -