Evidence map›Paper›PMID 34526592›Full record

ArticleScientific reports2021

Acute regional changes in myocardial strain may predict ventricular remodelling after myocardial infarction in a large animal model.

D S Mansell, V D Bruno, E Sammut, A Chiribiri, T Johnson, I Khaliulin, D Baz Lopez, H S Gill, K H Fraser, M Murphy and 5 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.4field-weighted citation impact, top 17% 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

8 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Article
  3. Intramyocardial immunomodulation with human CD16Frontiers in cardiovascular medicine · 2024
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
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

15 authors at 6 institutions in 1 country.

D S Mansell *Department of Mechanical Engineering, University of Bath, Bath, BA2 7AY, UK.
V D Bruno *Department of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
E SammutDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
A ChiribiriSchool of Biomedical Engineering and Imaging Sciences, King's College London, Westminster Bridge Road, London, SE1 7EH, UK.
T JohnsonDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
I KhaliulinDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
D Baz LopezDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
H S GillDepartment of Mechanical Engineering, University of Bath, Bath, BA2 7AY, UK.
K H FraserDepartment of Mechanical Engineering, University of Bath, Bath, BA2 7AY, UK.
M MurphyMRC Mitochondrial Biology Unit, The Keith Peters Building, Cambridge Biomedical Campus, Hills Road, Cambridge, CB2 0XY, UK.
T KriegDepartment of Medicine, University of Cambridge, Addenbrookes Hospital, Hills Rd, Box 157, Cambridge, CB2 0QQ, UK.
M S SuleimanDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
S GeorgeDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK.
R AscioneDepartment of Translational Science, Bristol Heart Institute and Translational Biomedical Research Centre, Faculty of Health Science, Bristol Royal Infirmary, Level 7, University of Bristol, Bristol, BS2 8HW, UK. R.Ascione@bristol.ac.uk.
A N CooksonDepartment of Mechanical Engineering, University of Bath, Bath, BA2 7AY, UK.
University of Bristol · GBUniversity of Bath · GBBristol Royal Infirmary · GBKing's College London · GBMRC Mitochondrial Biology Unit · GBUniversity of Cambridge · GB

Funding

British Heart Foundation FS/19/72/34698British Heart Foundation PG/18/49/33833Medical Research Council MC_EX_MR/M015769/1Medical Research Council MR/L012723/1Medical Research Council MR/M015769/1
6 · The paper itself

Abstract

To identify predictors of left ventricular remodelling (LVR) post-myocardial infarction (MI) and related molecular signatures, a porcine model of closed-chest balloon MI was used along with serial cardiac magnetic resonance imaging (CMRI) up to 5-6 weeks post-MI. Changes in myocardial strain and strain rates were derived from CMRI data. Tissue proteomics was compared between infarcted and non-infarcted territories. Peak values of left ventricular (LV) apical circumferential strain (ACS) changed over time together with peak global circumferential strain (GCS) while peak GLS epicardial strains or strain rates did not change over time. Early LVR post-MI enhanced abundance of 39 proteins in infarcted LV territories, 21 of which correlated with LV equatorial circumferential strain rate. The strongest associations were observed for D-3-phosphoglycerate dehydrogenase (D-3PGDH), cysteine and glycine-rich protein-2, and secreted frizzled-related protein 1 (sFRP1). This study shows that early changes in regional peak ACS persist at 5-6 weeks post-MI, when early LVR is observed along with increased tissue levels of D-3PGDH and sFRP1. More studies are needed to ascertain if the observed increase in tissue levels of D-3PGDH and sFRP1 might be casually involved in the pathogenesis of adverse LV remodelling.

Indexed as

Ventricular RemodelingAnimalsBiomarkersComputational BiologyData AnalysisData Interpretation, StatisticalDisease Models, AnimalDisease SusceptibilityFemaleImage Processing, Computer-AssistedMagnetic Resonance ImagingMyocardial InfarctionMyocardiumProteomeProteomicsReproducibility of ResultsBiomarkersProteome

Identifiers

PMID34526592
PMCPMC8443552
OpenAlexW3160839422

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.