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Understanding cardiac troponin part 1: avoiding troponinitis
  1. Richard Body1,2,3,
  2. Edward Carlton4
  1. 1 Cardiovascular Sciences Research Group, The University of Manchester, Manchester, UK
  2. 2 Emergency Department, Central Manchester University Hospitals Foundation NHS Trust, Manchester, UK
  3. 3 School of Healthcare Science, Manchester Metropolitan University, Manchester, UK
  4. 4 Emergency Department, North Bristol NHS Trust, Southmead Hospital, Bristol, UK
  1. Correspondence to Professor Richard Body, Emergency Department, Manchester Royal Infirmary, Oxford Road, Manchester M13 9WL, UK; richard.body{at}


Cardiac troponin (cTn) is a highly specific biomarker of myocardial injury and is central to the diagnosis of acute myocardial infarction (AMI). By itself, however, cTn cannot identify the cause of myocardial injury. ‘Troponinitis’ is the condition that leads clinicians to falsely assign a diagnosis of AMI based only on the fact that a patient has an elevated cTn concentration. There are many causes of myocardial injury other than AMI. Clinicians are required to differentiate myocardial injury caused by AMI from other causes.

In part 1 of this series on cTn, we provide a structured overview to help practising clinicians to interpret ‘positive’ cTn results appropriately. There are three core principles. First, when reviewing a cTn result, clinicians must carefully consider the clinical context. Only this can distinguish primary (termed type 1) AMI caused by coronary artery disease from secondary (termed type 2) AMI caused by another condition with an imbalance in the supply and demand of oxygen to the myocardium. Second, clinicians must consider the patient’s baseline condition in order to determine the presence or absence of factors that may predict a chronic cTn elevation. Third, clinicians should routinely use serial sampling to detect a change of cTn that is expected in patients with acute (rather than chronic) myocardial injury. Using these simple principles, clinicians can avoid underdiagnosis and overdiagnosis of AMI.

  • acute myocardial infarction
  • acute coronary syndromes
  • diagnosis
  • sensitivity and specificity
  • troponins
  • high sensitivity
  • emergency medicine

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  • Twitter @richardbody; @eddcarlton

  • Funding During the preparation of this manuscript, the National Institute for Health Research (NIHR) paid for protected research time covering the majority of Richard Body’s salary (ref PDF-2012-193).

  • Competing interests RB accepted provision of travel and accommodation to present at a scientific session and a symposium (respectively) sponsored by Randox Laboratories.

  • Provenance and peer review Commissioned; externally peer reviewed.