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Possible mechanisms behind cardiac troponin elevations

Journal article
Authors Ola Hammarsten
J. Mair
M. Mockel
B. Lindahl
A. S. Jaffe
Published in Biomarkers
Volume 23
Issue 8
Pages 725-734
ISSN 1354-750X
Publication year 2018
Published at Institute of Biomedicine, Department of Clinical Chemistry and Transfusion Medicine
Pages 725-734
Language en
Keywords Cardiac troponin I, cardiac troponin T, myocardial injury, release, reversible, necrosis, apoptosis, acute myocardial-infarction, acute coronary syndrome, creatine-kinase, skeletal-muscle, cardiomyocyte apoptosis, myotonic-dystrophy, enzyme, levels, cell-death, t levels, heart, Biotechnology & Applied Microbiology, Toxicology, einhardt ra, 1994, science, v263, p390, iong ma, 1974, circulation, v49, p283, eenbergen c, 1985, circulation research, v57, p864, hwartz p, 1984, american journal of pathology, v115, p349, neil pl, 1992, american journal of pathology, v140, p1097
Subject categories Cardiac and Cardiovascular Systems


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.

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