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Cardiac troponins: from myocardial infarction to chronic disease

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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, emphasizing 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, emphasizing 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.

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            Author and article information

            Affiliations
            [1 ]1 BHF Centre of Research Excellence, The Rayne Institute, Cardiovascular Division, King’s College London, London, UK;
            [2 ]2 Burdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford, UK;
            [3 ]3 Clinical Blood Sciences and Cardiology, St George’s University Hospitals NHS Trust and St George’s University of London, London, UK;
            [4 ]4 Department of Biomedical Science, University of Westminster, London, UK
            Author notes
            [* ] Corresponding author. BHF Centre of Research Excellence, The Rayne Institute, Cardiovascular Division, King's College London, St Thomas' Hospital, London SE1 7EH, UK. Tel: +44 20 7188 1008; fax: +44 20 7188 0970, E-mail: mike.marber@ 123456kcl.ac.uk
            Journal
            Cardiovasc Res
            Cardiovasc. Res
            cardiovascres
            Cardiovascular Research
            Oxford University Press
            0008-6363
            1755-3245
            December 2017
            14 September 2017
            14 September 2017
            : 113
            : 14
            : 1708-1718
            29016754 5852618 10.1093/cvr/cvx183 cvx183
            © The Author 2017. Published by Oxford University Press 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.

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            Pages: 11
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            Funding
            Funded by: Medical Research Council 10.13039/501100000265
            Award ID: G1000737
            Funded by: British Heart Foundation 10.13039/501100000274
            Award ID: TG/15/1/31518 and FS/15/13/31320
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