How is cardiac troponin released from injured myocardium?

TY - JOUR

T1 - How is cardiac troponin released from injured myocardium?

AU - Mair, Johannes

AU - Lindahl, Bertil

AU - Hammarsten, Ola

AU - Müller, Christian

AU - Giannitsis, Evangelos

AU - Huber, Kurt

AU - Möckel, Martin

AU - Plebani, Mario

AU - Thygesen, Kristian

AU - Jaffe, Allan S

AU - European Society of Cardiology (ESC) Study Group on Biomarkers in Cardiology of the Acute Cardiovascular Care Association (ACCA)

PY - 2018/9/1

Y1 - 2018/9/1

N2 - Cardiac troponin I and cardiac troponin T are nowadays the criterion biomarkers for the laboratory diagnosis of acute myocardial infarction due to their very high sensitivities and specificities for myocardial injury. However, still many aspects of their degradation, tissue release and elimination from the human circulation are incompletely understood. Myocardial injury may be caused by a variety of different mechanisms, for example, myocardial ischaemia, inflammatory and immunological processes, trauma, drugs and toxins, and myocardial necrosis is preceded by a substantial reversible prelethal phase. Recent experimental data in a pig model of myocardial ischaemia demonstrated cardiac troponin release into the circulation from apoptotic cardiomyocytes as an alternative explanation for clinical situations with increased cardiac troponin without any other evidence for myocardial necrosis. However, the comparably lower sensitivities of all currently available imaging modalities, including cardiac magnetic resonance imaging for the detection of particularly non-focal myocardial necrosis in patients, has to be considered for cardiac troponin test result interpretation in clinical settings without any other evidence for myocardial necrosis apart from increased cardiac troponin concentrations as well.

AB - Cardiac troponin I and cardiac troponin T are nowadays the criterion biomarkers for the laboratory diagnosis of acute myocardial infarction due to their very high sensitivities and specificities for myocardial injury. However, still many aspects of their degradation, tissue release and elimination from the human circulation are incompletely understood. Myocardial injury may be caused by a variety of different mechanisms, for example, myocardial ischaemia, inflammatory and immunological processes, trauma, drugs and toxins, and myocardial necrosis is preceded by a substantial reversible prelethal phase. Recent experimental data in a pig model of myocardial ischaemia demonstrated cardiac troponin release into the circulation from apoptotic cardiomyocytes as an alternative explanation for clinical situations with increased cardiac troponin without any other evidence for myocardial necrosis. However, the comparably lower sensitivities of all currently available imaging modalities, including cardiac magnetic resonance imaging for the detection of particularly non-focal myocardial necrosis in patients, has to be considered for cardiac troponin test result interpretation in clinical settings without any other evidence for myocardial necrosis apart from increased cardiac troponin concentrations as well.

KW - Journal Article

UR - http://www.scopus.com/inward/record.url?scp=85050525621&partnerID=8YFLogxK

U2 - 10.1177/2048872617748553

DO - 10.1177/2048872617748553

M3 - Journal article

C2 - 29278915

SN - 2048-8726

VL - 7

SP - 553

EP - 560

JO - European Heart Journal: Acute Cardiovascular Care

JF - European Heart Journal: Acute Cardiovascular Care

IS - 6

ER -