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Historical cardiac troponin concentrations in patients with suspected acute coronary syndrome
  1. Caelan Taggart,
  2. Andrew R Chapman
  1. Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, UK
  1. Correspondence to Dr Andrew R Chapman, The University of Edinburgh Centre for Cardiovascular Science, Edinburgh EH16 4SB, Edinburgh, UK; a.r.chapman{at}

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High-sensitivity cardiac troponin (hs-cTn) assays are the only guideline-recommended cardiac biomarker for diagnosis of myocardial infarction.1 Their integration into diagnostic pathways that permit the early rule-out of myocardial infarction has improved the efficiency of healthcare delivery without compromising safety.2 3 However, they have led to an increased detection of myocardial injury (troponin concentration over the 99th centile diagnostic threshold) in patients without myocardial infarction, which can cause diagnostic uncertainty.4 Typically, chronic elevations in cardiac troponin are observed in older patients, those with cardiovascular comorbidity including hypertension, ischaemic heart disease, valvular heart disease and structural heart disease, or those with non-cardiovascular comorbidity such as chronic kidney disease or myopathy (figure 1).

Figure 1

Causes of chronic elevation in cardiac troponin concentration.

As hs-cTn assays were first introduced into clinical practice over a decade ago, in the majority of healthcare settings with access to electronic care records, the results of previous cardiac troponin concentrations will be available. This may provide an opportunity to understand the context of individual patients’ repeat cardiac troponin concentrations. For example, this might allow a clinician to understand whether a low elevation in cardiac troponin concentration was ‘normal’ or ‘abnormal’ for that individual in the context of their cardiovascular status and comorbidity. This individualised assessment could be informative to guide further investigation and treatment.

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  • Twitter @CaelanTaggart, @chapdoc1

  • Contributors CT and ARC wrote the manuscript.

  • Funding This study was funded by the British Heart Foundation (FS/CRTF/21/2473).

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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