P4576Prognostic value of high-sensitivity troponin I measured by two assays in patients presenting with suspected myocardial infarction
Authors: Ludwig S , Soerensen N , Makarova N , Neumann J , Voigtlaender L , Hartikainen T , Blankenberg S , Westermann D , Zeller T , Schofer N 
Published: October 2019

Abstract

Background
Troponin is the gold-standard biomarker for diagnosing acute myocardial infarction (AMI). High-sensitivity assayed troponin has furthermore proven to be a promising biomarker for the prediction of future adverse cardiovascular events.

Objective
Aim of the current study was to assess and compare the prognostic value of a single troponin I measurement in patients with suspected AMI analysed by a novel high-sensitive Troponin I (hs-TnI) assay, promising detection of very low troponin I plasma levels, as well as by a well-established hs-TnI assay.

Methods
Data was derived from two prospective studies of patients presenting with suspected AMI to the emergency department. Hs-TnI was measured in a total of 2,312 patients using both a novel hs-TnI assay (1; Singulex Clarity cTnI) and a widely applied and approved hs-TnI assay (2; Abbott Diagnostics, ARCHITECT i1000SR). The prognostic impact for overall mortality of both hs-TnI assays was assessed in the total patient cohort as well as in the subgroups of patients with AMI (n=498) and without AMI (n=1,813). Kaplan-Meier analyses stratified by hs-TnI tertiles in each subgroup were performed. Moreover, prognostic impacts of both hs-TnI assays were analysed in a multiple adjusted cox regression model. We compared the performance of both hs-TnI assays in predicting adverse outcome using c-statistics. Median follow up time was 2.4 years.

Results
Patients with AMI presented with significantly higher hs-TnI values on admission. Unadjusted Kaplan-Meier analysis survival curves in the entire study population (Figure 1) as well as in the non-AMI subgroup indicated a significantly higher event-rate in the third tertiles of both hs-TnI assays for overall mortality. In contrast, irrespective of the used assay we found no association between troponin I plasma levels and overall mortality in the AMI group. Cox regression models revealed significant associations between hs-TnI and overall mortality in the entire study cohort (1: HR 1.17 [1.10–1.25], p<0.001; 2: HR 1.18 [1.11–1.26], p<0.001) and in the non-AMI subgroup (1: HR 1.39 [1.21–1.6], p<0.001; 2: 1.49 [1.28–1.74], p<0.001), but no significant association in the AMI subgroup (1: HR 1.02 [0.91–1.13], p=0.79; 2: 1.03 [0.93–1.3], p=0.55). The addition of hs-TnI to cardiovascular risk factors for the prediction of overall mortality led to a similar increment in the c-index by both hs-TnI assays of 0.014; p=0.034 (1) and 0.015; p=0.037 (2), respectively.
Figure 1. Overall mortality

Conclusion
Hs-TnI assayed on admission is an independent predictor of adverse outcome beyond conventional risk factors in patients presenting to the emergency department with suspected but ruled-out diagnosis of AMI. In patients with the established diagnosis of AMI hs-TnI is not predictive for adverse outcome. Our findings demonstrate the potential role of hs-TnI as a biomarker for risk prediction. Both assessed hs-TnI assays performed equally in predicting adverse events.