Evidence map›Paper›PMID 24337456›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2014

Release kinetics of circulating cardiac myosin binding protein-C following cardiac injury.

Diederik W D Kuster, Adriana Cardenas-Ospina, Lawson Miller, Christoph Liebetrau, Christian Troidl, Holger M Nef, Helge Möllmann, Christian W Hamm, Karen S Pieper, Kenneth W Mahaffey and 4 more

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 30 citations in OpenAlex.

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  6. Regulatory roles of PIWI-interacting RNAs in cardiovascular disease.American journal of physiology. Heart and circulatory physiology · 2025
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  15. Myocardial injury associated with transcatheter aortic valve implantation (TAVI).Clinical research in cardiology : official journal of the German Cardiac Society · 2016
    Review
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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

14 authors at 6 institutions in 3 countries.

Diederik W D KusterDepartment of Cell and Molecular Physiology, Health Sciences Division, Loyola University Chicago, Maywood, Illinois;
Adriana Cardenas-Ospina
Lawson Miller
Christoph Liebetrau
Christian Troidl
Holger M Nef
Helge Möllmann
Christian W Hamm
Karen S Pieper
Kenneth W Mahaffey
Neal S Kleiman
Bruno D Stuyvers
Ali J Marian
Sakthivel Sadayappan
Kerckhoff Klinik · DEMemorial University of Newfoundland · CAClinical Research Institute · USLoyola University Chicago · USHouston Methodist · USThe University of Texas Health Science Center at Houston · US

Funding

Fast myosin binding protein-C and cardiac contractility in heart failureR01HL105826 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2011 to 2025
$4.5M
Proteomic approaches to validate novel cardiac biomarkers for myocardial infarctiK02HL114749 · NHLBI · UNIVERSITY OF CINCINNATI · PI SADAYAPPAN, SAKTHIVEL · 2012 to 2016
$498k
CIHR 81150NHLBI NIH HHS K02 HL114749NHLBI NIH HHS K02HL-114749NHLBI NIH HHS R01 HL105826NHLBI NIH HHS R01HL-105826
6 · The paper itself

Abstract

Diagnosis of myocardial infarction (MI) is based on ST-segment elevation on electrocardiographic evaluation and/or elevated plasma cardiac troponin (cTn) levels. However, troponins lack the sensitivity required to detect the onset of MI at its earliest stages. Therefore, to confirm its viability as an ultra-early biomarker of MI, this study investigates the release kinetics of cardiac myosin binding protein-C (cMyBP-C) in a porcine model of MI and in two human cohorts. Release kinetics of cMyBP-C were determined in a porcine model of MI (n = 6, pigs, either sex) by measuring plasma cMyBP-C level serially from 30 min to 14 days after coronary occlusion, with use of a custom-made immunoassay. cMyBP-C plasma levels were increased from baseline (76 ± 68 ng/l) at 3 h (767 ± 211 ng/l) and peaked at 6 h (2,418 ± 780 ng/l) after coronary ligation. Plasma cTnI, cTnT, and myosin light chain-3 levels were all increased 6 h after ligation. In a cohort of patients (n = 12) with hypertrophic obstructive cardiomyopathy undergoing transcoronary ablation of septal hypertrophy, cMyBP-C was significantly increased from baseline (49 ± 23 ng/l) in a time-dependent manner, peaking at 4 h (560 ± 273 ng/l). In a cohort of patients with non-ST segment elevation MI (n = 176) from the SYNERGY trial, cMyBP-C serum levels were significantly higher (7,615 ± 4,514 ng/l) than those in a control cohort (416 ± 104 ng/l; n = 153). cMyBP-C is released in the blood rapidly after cardiac damage and therefore has the potential to positively mark the onset of MI.

Indexed as

AnimalsBiomarkersCarrier ProteinsDisease Models, AnimalHumansKineticsMyocardial InfarctionMyosin Binding Protein CSwineTroponin ITroponin TBiomarkersCarrier ProteinsMyosin Binding Protein CTroponin ITroponin Tacute coronary syndromebiomarkercardiac troponin IcMyBP-CMYBPC3myocardial infarction

Identifiers

PMID24337456
PMCPMC3920245
OpenAlexW2147654984

What OpenQuestion holds

Textmetadata
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.