False positives and false negatives can be due to non-repeatable "flyers" or native antibody interference that are assay specific. Interestingly, the decision regarding whether to measure either hs-cTnT or hs-cTnI in the acute setting is not typically a clinical decision per se. Due to patent, hs-cTnT assays are available from only one manufacturer Roche Diagnostics. Therefore, the primary supplier to the local biochemistry laboratory often dictates which of hs-cTnI or hs-cTnT is measured for patient care.
It is rare for both hs-cTnT and hs-cTnI to be measured in the same study cohort, and clinicians are often experienced in the clinical interpretation of either hs-cTn assay result but not both. In the acute setting, the available data suggest that hs-cTn assays perform very similarly in clinical care. The Advantageous Predictors of Acute Coronary Syndromes Evaluation APACE study group hypothesized that combining the two biochemical signals from hs-cTnT and hs-cTnI might overcome preanalytical, analytical, and pathophysiological differences between the biomarkers and improve clinical decision-making.
The area under the curve diagnostic accuracy for both assays at presentation was 0. Further study of the Siemens hs-cTnI assay showed similar diagnostic performance. Overall, the assays perform similarly, suggesting that acute myocardial injury drives circulating concentrations of both cTn in this setting. Despite apparent broad concordance between troponin assays in the acute setting, strong emerging evidence in the general population suggests that cTnT and cTnI differ meaningfully in their association with disease outcomes.
This has led to interest in use of the troponin assays not just in the acute setting but also for cardiovascular disease CVD risk prediction. In previous cohort studies, one of hs-cTnI or hs-cTnT but rarely both had been measured, presumably led by a presumed inter-changeability of assays in the acute setting. This has yielded an evidence base lacking direct evidence as to which biomarker might actually be preferable. This is reflected in our recent study-level meta-analysis, where 13 studies measured cTnI and 7 studies measured cTnT; none measured both.
The cross-sectional Maastricht study provides preliminary evidence that troponin assays may not be interchangeable in the general population. Clearly, in most biological situations this is a notable correlation, but it is a long way from being considered interchangeable for assays supposedly measuring the same biomarker. In cross-sectional data, hs-cTnT and hs-cTnI were detectable in Figure 2.
Both troponins had strong univariable associations with CVD outcomes, indicating that circulating levels were probably to some degree related to myocardial injury Figure 3, left panels.
However, after adjusting for traditional CVD risk factors, the strength of the association attenuated for both troponins Figure 3, right panels such that the hazard ratio for a 1 standard deviation increase in log troponin was 1. Figure 3. As a final examination of the possible distinct natures of hs-cTnT and hs-cTnI, we can use genetics to identify potential upstream causes of troponin extrusion into the circulation. Inheritance of specific allelic variants is random at a population level and therefore not confounded by lifestyle risk factors and circumstance and is not subject to reverse causality.
These genes encode proteins that are both part of the kallikrein-kinin axis and have shown associations with other vasoactive peptides such as B-type natriuretic peptide. However, these genetic signals were not associated with hs-cTnT. This provides at least some evidence that the genetic determinants of the cTn might not overlap, although larger-scale meta-analyses are required to look at this issue in more detail.
The simplest explanation as to why the two cTn appear very similar in the acute setting is that any signal not related to acute cardiomyocyte death or injury is diluted by the overpowering signal derived from the ongoing event. Therefore, most of the cTn I or T in the circulation can be attributed to the cardiomyocyte injury. Compared with conventional troponin testing, high sensitivity troponin I testing identifies more patients with ACS but is not associated with improved outcomes.
Conventional troponin testing can miss some patients with acute coronary syndrome ACS , especially single tests performed early in the disease course. Use of high-sensitivity troponin I hsTnI testing can reduce missed cases but may decrease specificity. These authors evaluated whether use of an hsTnI assay affected the combined outcome of subsequent myocardial infarction or death at 1 year in nearly 48, patients with suspected ACS at 10 hospitals in Scotland.
Patients underwent simultaneous conventional and hsTnI testing; hsTnI results were concealed from treating physicians for approximately 19, patients in a cluster-randomized, stepped-wedge fashion. The 1-year outcome did not differ significantly when treating physicians had access to hsTnI results compared to when they did not have access adjusted odds ratio, 1.
Median length of stay increased for reclassified patients when hsTnI results were available to physicians from 21 to 51 hours but decreased for those without myocardial injury from 7 to 4 hours. For now, without very specific agreement from my cardiology colleagues, I am not changing practice.
Shah ASV et al. High-sensitivity troponin in the evaluation of patients with suspected acute coronary syndrome: A stepped-wedge, cluster-randomised controlled trial.
Lancet Aug 28; [e-pub]. Lancet Aug 28 Compared with conventional troponin testing, high sensitivity troponin I testing identifies more patients with ACS but is not associated with improved outcomes. Citation s : Shah ASV et al.
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