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Cardiac troponins: from myocardial infarction to chronic disease

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-re...

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Autores principales: Park, Kyung Chan, Gaze, David C, Collinson, Paul O, Marber, Michael S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Oxford University Press 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852618/
https://www.ncbi.nlm.nih.gov/pubmed/29016754
http://dx.doi.org/10.1093/cvr/cvx183
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author Park, Kyung Chan
Gaze, David C
Collinson, Paul O
Marber, Michael S
author_facet Park, Kyung Chan
Gaze, David C
Collinson, Paul O
Marber, Michael S
author_sort Park, Kyung Chan
collection PubMed
description 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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spelling pubmed-58526182018-03-23 Cardiac troponins: from myocardial infarction to chronic disease Park, Kyung Chan Gaze, David C Collinson, Paul O Marber, Michael S Cardiovasc Res Review 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. Oxford University Press 2017-12 2017-09-14 /pmc/articles/PMC5852618/ /pubmed/29016754 http://dx.doi.org/10.1093/cvr/cvx183 Text en © The Author 2017. Published by Oxford University Press on behalf of the European Society of Cardiology http://creativecommons.org/licenses/by/4.0/ 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.
spellingShingle Review
Park, Kyung Chan
Gaze, David C
Collinson, Paul O
Marber, Michael S
Cardiac troponins: from myocardial infarction to chronic disease
title Cardiac troponins: from myocardial infarction to chronic disease
title_full Cardiac troponins: from myocardial infarction to chronic disease
title_fullStr Cardiac troponins: from myocardial infarction to chronic disease
title_full_unstemmed Cardiac troponins: from myocardial infarction to chronic disease
title_short Cardiac troponins: from myocardial infarction to chronic disease
title_sort cardiac troponins: from myocardial infarction to chronic disease
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5852618/
https://www.ncbi.nlm.nih.gov/pubmed/29016754
http://dx.doi.org/10.1093/cvr/cvx183
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