CoChat
Sign Up
Cited by 510Acute Myocardial Infarction ResearchCardiac Imaging and DiagnosticsTakotsubo Cardiomyopathy and Associated Phenomena

The DOI matches its Crossref record; 103 of the 105 references it cites were found in a registry or an index.

Cardiac troponins: from myocardial infarction to chronic disease

Open access
Park, Kyung Chan, Gaze, David C, Collinson, Paul O, Marber, Michael S·2017·Cardiovascular Research
DOI 10.1093/cvr/cvx183PMC PMC5852618
Open this paper in CoChat — free accountOpen PDF

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.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1093/cvr/cvx183

Cites

103 of 103 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Flagged first, then by citations

Show all 105 references

2 of the 105 references couldn’t be matched to a known paper.

Research works printed but not linked: 2

  1. Bernard, 1979, Nomenclature and criteria for diagnosis of ischaemic heart disease, Circulation, 59, 607
  2. Vasile, 2009, The biological basis of troponin in heart disease: possible uses for troponin fragmentology, Heart Metab, 43, 5

Cited by

Sorted by citations

Items 301–400 of 509

Related

See all

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
ORCID
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
DOI
10.1093/cvr/cvx183
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
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 ›

Are you an author, or do you see a problem with this page? Request a review