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Cardiac troponins: from myocardial infarction to chronic disease.

Park, KC; Gaze, DC; Collinson, PO; Marber, MS (2017) Cardiac troponins: from myocardial infarction to chronic disease. Cardiovasc Res, 113 (14). pp. 1708-1718. ISSN 1755-3245 https://doi.org/10.1093/cvr/cvx183
SGUL Authors: Collinson, Paul

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Abstract

Elucidation of the physiologically distinct subunits of troponin in 1973 greatly facilitated our understanding of cardiac contraction. Although troponins are expressed in both skeletal and cardiac muscle, there are isoforms of troponin I/T expressed selectively in the heart. By exploiting cardiac-restricted epitopes within these proteins, one of the most successful diagnostic tests to-date has been developed: cardiac troponin (cTn) assays. For the past decade, cTn has been regarded as the gold-standard marker for acute myocardial necrosis: the pathological hallmark of acute myocardial infarction (AMI). Whilst cTn is the cornerstone for ruling-out AMI in patients presenting with a suspected acute coronary syndrome (ACS), elevated cTn is frequently observed in those without clinical signs indicative of AMI, often reflecting myocardial injury of 'unknown origin'. cTn is commonly elevated in acute non-ACS conditions, as well as in chronic diseases. It is unclear why these elevations occur; yet they cannot be ignored as cTn levels in chronically unwell patients are directly correlated to prognosis. Paradoxically, improvements in assay sensitivity have meant more differential diagnoses have to be considered due to decreased specificity, since cTn is now more easily detected in these non-ACS conditions. It is important to be aware cTn is highly specific for myocardial injury, which could be attributable to a myriad of underlying causes, emphasising the notion that cTn is an organ-specific, not disease-specific biomarker. Furthermore, the ability to detect increased cTn using high-sensitivity assays following extreme exercise is disconcerting. It has been suggested troponin release can occur without cardiomyocyte necrosis, contradicting conventional dogma, emphasising a need to understand the mechanisms of such release. This review discusses basic troponin biology, the physiology behind its detection in serum, its use in the diagnosis of AMI, and some key concepts and experimental evidence as to why cTn can be elevated in chronic diseases.

Item Type: Article
Additional Information: © The Author 2017. Published on behalf of the European Society of Cardiology. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.
Keywords: Cardiovascular System & Hematology, 1102 Cardiovascular Medicine And Haematology
SGUL Research Institute / Research Centre: Academic Structure > Molecular and Clinical Sciences Research Institute (MCS)
Academic Structure > Molecular and Clinical Sciences Research Institute (MCS) > Cardiac (INCCCA)
Journal or Publication Title: Cardiovasc Res
ISSN: 1755-3245
Language: eng
Dates:
DateEvent
December 2017Published
14 September 2017Published Online
12 September 2017Accepted
Publisher License: Creative Commons: Attribution 4.0
Projects:
Project IDFunderFunder ID
G1000737Medical Research Councilhttp://dx.doi.org/10.13039/501100000265
R060701Guy's and St Thomas' Charityhttp://dx.doi.org/10.13039/501100000380
R100404Guy's and St Thomas' Charityhttp://dx.doi.org/10.13039/501100000380
TG/15/1/31518British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
FS/15/13/31320British Heart Foundationhttp://dx.doi.org/10.13039/501100000274
UNSPECIFIEDNational Institute for Health Researchhttp://dx.doi.org/10.13039/501100000272
PubMed ID: 29016754
Go to PubMed abstract
URI: https://openaccess.sgul.ac.uk/id/eprint/109225
Publisher's version: https://doi.org/10.1093/cvr/cvx183

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