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Crit Care. 2017 Aug 16;21(1):216. doi: 10.1186/s13054-017-1800-4.

Early troponin I in critical illness and its association with hospital mortality: a cohort study.

Author information

1
Department of Anaesthesia, Critical Care and Pain Medicine, University of Edinburgh, Royal Infirmary Edinburgh, 2nd Floor Anaesthetics Corridor, Edinburgh, EH16 4SA, UK. annemarie.docherty@ed.ac.uk.
2
Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK. annemarie.docherty@ed.ac.uk.
3
Academic Unit of Anaesthesia, Pain & Critical Care, University of Glasgow, Glasgow, UK.
4
Department of Critical Care, King's College London, Guys and St Thomas' Hospital, London, UK.
5
Internal Medicine Department, Hospital Jose Joaquim Fernandes, Beja, Portugal.
6
Department of Anaesthesia, Critical Care and Pain Medicine, University of Edinburgh, Royal Infirmary Edinburgh, 2nd Floor Anaesthetics Corridor, Edinburgh, EH16 4SA, UK.
7
Centre for Inflammation Research, University of Edinburgh, Edinburgh, UK.
8
Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, UK.

Abstract

BACKGROUND:

Troponin I (TnI) is frequently elevated in critical illness, but its interpretation is unclear. Our primary objectives in this study were to evaluate whether TnI is associated with hospital mortality and if this association persists after adjusting for potential confounders. We also aimed to ascertain whether addition of TnI to the Acute Physiological and Chronic Health Evaluation II (APACHE II) risk prediction model improves its performance in general intensive care unit (ICU) populations.

METHODS:

We performed an observational cohort study with independent derivation and validation cohorts in two general level 3 ICU departments in the United Kingdom. The derivation cohort was a 4.5-year cohort (2010-2014) of general ICU index admissions (n = 1349). The validation cohort was used for secondary analysis of a prospective study dataset (2010) (n = 145). The primary exposure was plasma TnI concentration taken within 24 h of ICU admission. The primary outcome was hospital mortality. We performed multivariate regression, adjusting for components of the APACHE II model. We derived the risk prediction score from the multivariable model with TnI.

RESULTS:

Hospital mortality was 37.3% (n = 242) for patients with detectable TnI, compared with 14.6% (n = 102) for patients without detectable TnI. There was a significant univariate association between TnI and hospital mortality (OR per doubling TnI 1.16, 95% CI 1.13-1.20, p < 0.001). This persisted after adjustment for APACHE II model components (TnI OR 1.05, 95% CI 1.01-1.09, p = 0.003). TnI correlated most strongly with the acute physiology score (APS) component of APACHE II (r = 0.39). Addition of TnI to the APACHE II model did not improve discrimination (APACHE II concordance statistic [c-index] 0.835, 95% CI 0.811-0.858; APACHE II + TnI c-index 0.837, 95% CI 0.813-0.860; p = 0.330) or other measures of model performance.

CONCLUSIONS:

TnI is an independent predictor of hospital mortality and correlates most highly with the APS component of APACHE II. It does not improve risk prediction. We would not advocate the adoption of routine troponin analysis on admission to ICU, and we recommend that troponin be measured only if clinically indicated.

KEYWORDS:

Critical care; Hospital mortality; Troponin

PMID:
28814347
PMCID:
PMC5559840
DOI:
10.1186/s13054-017-1800-4
[Indexed for MEDLINE]
Free PMC Article

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