Possible mechanisms behind cardiac troponin elevations

Ola Hammarsten, Johannes Mair, Martin Möckel, Bertil Lindahl, Allan S. Jaffe

Research output: Contribution to journalReview articlepeer-review

29 Scopus citations


Abstract: Cardiac-specific troponins are elevated in blood following cardiac injury and are the preferred diagnostic biomarkers when acute myocardial infarction is suspected clinically. Cardiac troponin (cTn) elevations are also observed in clinical conditions without obvious connection to cardiac injury. Irrespective of the underlying condition, cTn elevation is linked to a poor prognosis, even if the elevation is stable over time. Here, we explore mechanisms that may lead to cTn elevations, including necrosis, apoptosis, necroptosis, cell wounds and decreased clearance. The aim is to broaden the perspective of how we interpret unexpected cTn elevations in patients. The cTn elevations may not be able to serve as direct proof of myocardial necrosis especially in the absence of a clear-cut reason for its release. Abbreviations: AMI: acute myocardial infarction; cTn: cardiac troponin; cTnI: cardiac troponin I; cTnT: cardiac troponin T; MLKL: mixed lineage kinase domain-like; TUNEL: terminal deoxynucleotidyl transferase nick end labeling.

Original languageEnglish (US)
Pages (from-to)725-734
Number of pages10
Issue number8
StatePublished - Nov 17 2018


  • Cardiac troponin I
  • apoptosis
  • cardiac troponin T
  • clearance
  • myocardial injury
  • necrosis
  • release
  • reversible

ASJC Scopus subject areas

  • Biochemistry
  • Clinical Biochemistry
  • Health, Toxicology and Mutagenesis


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