Evidence map›Paper›PMID 29016754›Full record

ReviewCardiovascular research2017

Cardiac troponins: from myocardial infarction to chronic disease.

Kyung Chan Park, David C Gaze, Paul O Collinson, Michael S Marber

Open access · hybridAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 252 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
252citing papers in PubMed, 4 pooled it
24.1field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

252 citing papers in PubMed, 4 syntheses or guidelines pooled it, 500 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Pooled it
  5. Trial
  6. Modelling the cost-effectiveness of person-centred care for patients with acute coronary syndrome.The European journal of health economics : HEPAC : health economics in prevention and care · 2020
    Trial
  7. Article
  8. Review
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  13. Cardiac Biomarkers in Chronic Kidney Disease: Signal or Noise?Clinical journal of the American Society of Nephrology : CJASN · 2026
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
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  20. Article

192 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 3 institutions in 1 country.

Kyung Chan ParkBHF Centre of Research Excellence, The Rayne Institute, Cardiovascular Division, King's College London, London, UK.
David C GazeClinical Blood Sciences and Cardiology, St George's University Hospitals NHS Trust and St George's University of London, London, UK.
Paul O CollinsonClinical Blood Sciences and Cardiology, St George's University Hospitals NHS Trust and St George's University of London, London, UK.
Michael S MarberBHF Centre of Research Excellence, The Rayne Institute, Cardiovascular Division, King's College London, London, UK.
King's College London · GBSt George’s University Hospitals NHS Foundation Trust · GBSt George's, University of London · GB

Funding

British Heart Foundation FS/15/13/31320British Heart Foundation TG/15/1/31518Medical Research Council G1000737
6 · The paper itself

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.

Indexed as

Acute Coronary SyndromeAnimalsBiomarkersChronic DiseaseHumansMyocardial InfarctionMyocardiumTroponin TBiomarkersTroponin TBiomarkerCardiac troponinChronic diseasePrognosisRelease mechanism

Identifiers

PMID29016754
PMCPMC5852618
OpenAlexW2755269296

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.