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Cardiac troponins and prediction of coronary artery disease risk
  1. Anoop Dinesh Shah1,2
  1. 1Institute of Health Informatics, University College London, London, UK
  2. 2Department of General Medicine, University College London Hospitals NHS Foundation Trust, London, UK
  1. Correspondence to Dr Anoop Dinesh Shah, Farr Institute of Health Informatics Research, UCL Institute of Health Informatics, University College London, 222 Euston Road, London NW1 2DA, UK; anoop{at}

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Cardiac troponins are proteins found in cardiac muscle cells, which can be released into the bloodstream as a result of myocardial injury. Their detection in the blood has been used for over 15 years to aid the diagnosis of myocardial infarction. Troponin forms a part of the troponin–tropomyosin complex that regulates cardiac muscle contraction, and consists of three subunits: troponin T, which binds to tropomyosin; troponin C, which binds calcium ions; and troponin I, which is the inhibitory subunit. When the complex is activated by calcium ions, the tropomysin strands move to reveal myosin-binding sites on the actin filaments, initiating muscle contraction.1

Assays for troponins I and T are in routine clinical use for measuring their concentration in the blood. Detection of a rise (and fall) in troponin is a key component of the current universal definition of myocardial infarction, and troponins are used clinically to differentiate acute coronary syndromes into unstable angina (no troponin release) and myocardial infarction (cardiac muscle damage due to ischaemia).2 However, a range of other cardiac conditions (such as cardiomyopathies, arrhythmias and heart failure) and non-cardiac conditions (such as hypoxia, sepsis, pulmonary embolism, renal failure, stroke and strenuous exercise) may also cause a rise in troponin. …

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  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.

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