TROPonin I in Cardiovascular patients in CriticAL care. A
multicentre prospective observational cohort study: preliminary
results.
A Docherty1, N Lone1, S Stanworth2, T Walsh1
Department of Critical Care, University of Edinburgh, Edinburgh,
UK
Department of Haematology, John Radcliffe Hospital, Oxford, UK
annemarie.docherty@ed.ac.uk
Critical illness increases myocardial work and may impair coronary
artery perfusion. This is particularly relevant in patients with
cardiovascular disease (CVD) and may result in an oxygen supplydemand imbalance, and “Type 2” MI (1). The diagnosis of
myocardial infarction in critically ill patients is subjective, and
understanding the dynamics of quantitative biomarkers is key to the
diagnosis. Troponin release is prevalent in the critically ill and is
associated with higher mortality (2,3). We aimed to describe and
quantify the pattern of Troponin I release in critically ill patients with
cardiovascular disease.
Methods
Ethics approval was by Scotland A REC, and Newcastle REC.
Patients with cardiovascular disease were recruited at admission to
critical care in 6 sites in Scotland and England, and followed up for
six months. Troponin I (Abbott Highly Sensitive Architect Stat assay)
and other biomarkers, haemodynamic parameters, and ECGs were
collected daily for a maximum of 10 days, in addition to
cardiovascular events and blood transfusion data. Here we present log
Troponin I as the outcome (Study outcomes were adverse
cardiovascular events, and mortality). We analysed the data using
linear multilevel analysis in R and MLwiN.
Results
There were 49 patients recruited at the time of submission, median
age 74 (IQR 66-79), 86% male. The median Sequential Organ Failure
Assessment (SOFA) score was 5 (3-8). Peak Troponin I 74ng/l (31284). Respiratory, cardiac and renal components of SOFA, and age
were all significant independent predictors of log troponin I (p<0.05).
ECG analysis (first 10 patients only): baseline 7/10 abnormal, 8/10
had dynamic changes including ST elevation, ST depression, and Tw
inversion. There were 3 clinically identified Myocardial Infarctions.
Day of ICU admission
Figure 1: Patterns of Troponin I release for individual patients from
day of ICU admission
Discussion
The rise and fall pattern of Troponin I release, preceded by significant
cardio-respiratory compromise, in addition to the peak at Day 2-3
suggest that myocardial infarction may be under-diagnosed in critical
illness in this high risk population. We hope to quantify myocardial
injury in this population using a larger cohort.
1.Thygesen K, Alpert J, Jaffe A, Simoons M. Third universal definition of
myocardial infarction. JACC Cardiovasc Interv. 2012;60(16):1581–98.
2.VISION Group. Association Between Postoperative Troponin and 30-Day
Mortality Among Patients Undergoing Noncardiac Surgery.
2012;307(21):2295–304.
3.Ostermann M, Lo J, Toolan M, et al. A prospective study of the impact of
serial troponin measurements on the diagnosis of myocardial infarction and
hospital and six-month mortality in patients admitted to ICU with non-cardiac
diagnoses. Crit Care [Internet]. Critical Care; 2014 Jan;18(2):R62.