Myocardial Injury in Critically Ill Patients with Community-acquired Pneumonia: A Cohort Study

Publication date

2019-05

Authors

Frencken, Jos F.ISNI 000000039124204X
van Baal, Lottie
Kappen, Teus H.ORCID 0000-0003-1895-0998ISNI 0000000394235275
Donker, Dirk
Horn, Janneke
van der Poll, Tom
van Klei, Wilton AISNI 0000000396755004
Bonten, Marc J MISNI 0000000034264654
Cremer, Olaf L.ORCID 0000-0003-4264-1108ISNI 0000000387039874
MARS Consortium

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Advisors

Supervisors

Document Type

Article

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License

taverne

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.

Keywords

Community-acquired pneumonia, Etiology, Myocardial injury, Sepsis, Taverne, Pulmonary and Respiratory Medicine

Citation

Frencken, J F, van Baal, L, Kappen, T H, Donker, D W, Horn, J, van der Poll, T, van Klei, W A, Bonten, M J M, Cremer, O L & MARS Consortium 2019, 'Myocardial Injury in Critically Ill Patients with Community-acquired Pneumonia : A Cohort Study', Annals of the American Thoracic Society, vol. 16, no. 5, pp. 606-612. https://doi.org/10.1513/AnnalsATS.201804-286OC