Evidence mapPaperPMID 37939716Full record

ArticleESC heart failure2024

Phenotyping patients with ischaemic heart disease at risk of developing heart failure: an analysis of the HOMAGE trial.

Diogo Santos-Ferreira, Sílvia O Diaz, João Pedro Ferreira, Nicolas Girerd, Pierpaolo Pellicori, Beatrice Mariottoni, Franco Cosmi, Mark Hazebroek, Job A J Verdonschot, Joe Cuthbert and 10 more

Open access · goldAbstract read
In one paragraph

Article in ESC heart failure, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

7 citing papers in PubMed, 7 citations in OpenAlex.

  1. Trial
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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

20 authors at 9 institutions in 10 countries.

Diogo Santos-FerreiraDepartment of Cardiology, Centro Hospitalar Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal.ORCID https://orcid.org/0000-0003-1428-1651
Sílvia O DiazDepartment of Surgery and Physiology, Cardiovascular R&D Centre - UnIC@RISE, Faculty of Medicine of the University of Porto, Porto, Portugal.
João Pedro FerreiraDepartment of Surgery and Physiology, Cardiovascular R&D Centre - UnIC@RISE, Faculty of Medicine of the University of Porto, Porto, Portugal.
Nicolas GirerdInserm, Centre d'Investigation Clinique Plurithématique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Université de Lorraine, Nancy, France.
Pierpaolo PellicoriSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK.
Beatrice MariottoniDepartment of Cardiology, Cortona Hospital, Arezzo, Italy.
Franco CosmiInserm, Centre d'Investigation Clinique Plurithématique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Université de Lorraine, Nancy, France.
Mark HazebroekDepartment of Cardiology, Maastricht University Medical Center, Maastricht, The Netherlands.
Job A J VerdonschotDepartment of Cardiology, Maastricht University Medical Center, Maastricht, The Netherlands.
Joe CuthbertDepartment of Cardiology, University of Hull, Castle Hill Hospital, Cottingham, UK.
Johannes PetutschniggDepartment of Internal Medicine and Cardiology, Charité University Medicine, Berlin Institute of Health (BIH), and German Centre for Cardiovascular Research (DZHK), Partner Site Berlin, Berlin, Germany.
Stephane HeymansDepartment of Cardiology, Maastricht University Medical Center, Maastricht, The Netherlands.
Jan A StaessenNon-Profit Research Association Alliance for the Promotion of Preventive Medicine (APPREMED), Mechelen, Belgium.
Burkert PieskeDepartment of Internal Medicine and Cardiology, Charité University Medicine, Berlin Institute of Health (BIH), and German Centre for Cardiovascular Research (DZHK), Partner Site Berlin, Berlin, Germany.
Frank EdelmannDepartment of Internal Medicine and Cardiology, Charité University Medicine, Berlin Institute of Health (BIH), and German Centre for Cardiovascular Research (DZHK), Partner Site Berlin, Berlin, Germany.
Andrew L ClarkDepartment of Cardiology, University of Hull, Castle Hill Hospital, Cottingham, UK.
Patrick RossignolInserm, Centre d'Investigation Clinique Plurithématique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Université de Lorraine, Nancy, France.
Ricardo Fontes-CarvalhoDepartment of Cardiology, Centro Hospitalar Vila Nova de Gaia/Espinho, Vila Nova de Gaia, Portugal.
John G F ClelandSchool of Cardiovascular and Metabolic Health, University of Glasgow, Glasgow, UK.
Faiez ZannadInserm, Centre d'Investigation Clinique Plurithématique 1433, CHRU de Nancy, F-CRIN INI-CRCT, Université de Lorraine, Nancy, France.
Inserm · FRUniversidade do Porto · PTUniversity Medical Center · USGerman Centre for Cardiovascular Research · DEUniversity of Glasgow · GBUniversity of Hull · GBAzienda Usl 8 Arezzo · ITChinese Preventive Medicine Association · CNDeutsches Herzzentrum der Charité · DE

Funding

British Heart Foundation Centre of Research Excellence RE/18/6/34217European Regional Development Fund (ERDF) NORTE-01-0145-FEDER-000039European Union 7th Framework Programme for Research and Technological Development 305507
6 · The paper itself

Abstract

aimsWe aim to characterize the clinical and proteomic profiles of patients at risk of developing heart failure (HF), with and without coronary artery disease (CAD) or prior myocardial infarction (MI). METHODS AND

resultsHOMAGE evaluated the effect of spironolactone on plasma and serum markers of fibrosis over 9 months of follow-up in participants with (or at risk of having) CAD, and raised natriuretic peptides. In this post hoc analysis, patients were classified as (i) neither CAD nor MI; (ii) CAD; or (iii) MI. Proteomic between-group differences were evaluated through logistic regression and narrowed using backward stepwise selection and bootstrapping. Among the 527 participants, 28% had neither CAD or MI, 31% had CAD, and 41% had prior MI. Compared with people with neither CAD nor MI, those with CAD had higher baseline plasma concentrations of matrix metalloproteinase-7 (MMP-7), galectin-4 (GAL4), plasminogen activator inhibitor 1 (PAI-1), and lower plasma peptidoglycan recognition protein 1 (PGLYRP1), whilst those with a history of MI had higher plasma MMP-7, neurotrophin-3 (NT3), pulmonary surfactant-associated protein D (PSPD), and lower plasma tumour necrosis factor-related activation-induced cytokine (TRANCE). Proteomic signatures were similar for patients with CAD or prior MI. Treatment with spironolactone was associated with an increase of MMP7, NT3, and PGLYRP1 at 9 months.

conclusionsIn patients at risk of developing HF, those with CAD or MI had a different proteomic profile regarding inflammatory, immunological, and collagen catabolic processes.

Indexed as

Coronary Artery DiseaseHeart FailureMyocardial InfarctionHumansMatrix Metalloproteinase 7ProteomicsSpironolactoneMatrix Metalloproteinase 7SpironolactoneCoronary artery diseaseHeart failureMyocardial infarctionProteomicsSpironolactone

Identifiers

PMID37939716
PMCPMC10804163
OpenAlexW4388482907

What Socratic holds

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LicenceCC BY
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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 Socratic graph.