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Cardiac troponins: from myocardial infarction to chronic disease
Open accessAbstract
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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“Cardiac troponin I (cTnI) is a gold-standard biomarker for cardiovascular diseases (the leading cause of death worldwide)22–25.”
From Nanoproteomics enables proteoform-resolved analysis of low-abundance proteins in human serum (2020) · cites this paper as [25]
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“Note that the estimated levels of cTnI released after cardiac injury events such as AMI are typically in the range of 0.5–50 ng/mL25,27.”
From Nanoproteomics enables proteoform-resolved analysis of low-abundance proteins in human serum (2020) · cites this paper as [25]
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Metadata
- Authors
- Park, K. C., Gaze, D. C., Collinson, P. O., & Marber, M. S.
- Affiliations
- King's College London (GB)
- St George's, University of London (GB)
- Corresponding author
- Marber, Michael S
- Venue
- Cardiovascular Research
- Publisher
- Oxford University Press (OUP)
- Published
- 2017-09-14
- Volume
- 113
- Issue
- 14
- Pages
- 1708-1718
- ISSN
- 0008-6363 (ISSN-L)
- 1755-3245
- PMC
- PMC5852618
- OpenAlex
- W2755269296
- Cited by
- 510
- References
- 105
- Citations by year
- 2026: 41 · 2025: 59 · 2024: 80 · 2023: 53 · 2022: 70 · 2021: 74 · 2020: 70 · 2019: 49 · 2018: 12 · 2017: 2
- FWCI
- 5.12
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Cardiovascular Research (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- St George's Online Research Archive (St George's University of London) (acceptedVersion)
- WestminsterResearch (University of Westminster) (acceptedVersion, cc-by)
- Funders
- Medical Research Council (G1000737)
- British Heart Foundation (TG/15/1/31518 and FS/15/13/31320)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Acute Myocardial Infarction Research
- Health Sciences › Medicine › Radiology, Nuclear Medicine and Imaging › Cardiac Imaging and Diagnostics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Takotsubo Cardiomyopathy and Associated Phenomena
- Keywords
- cardiac troponin, troponin I, troponin T, acute myocardial infarction, acute coronary syndrome, myocardial injury, high-sensitivity troponin assays, chronic disease, cardiac contraction
- MeSH terms
- Animals, Chronic Disease, Humans, Myocardial Infarction, Myocardium, Biomarkers, Troponin T, Acute Coronary Syndrome
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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