Evidence map›Paper›PMID 32458320›Full record

ArticleCardiovascular drugs and therapy2021

Factor Xa Inhibition with Apixaban Does Not Influence Cardiac Remodelling in Rats with Heart Failure After Myocardial Infarction.

Salva R Yurista, Herman H W Silljé, Kirsten T Nijholt, Martin M Dokter, Dirk J van Veldhuisen, Rudolf A de Boer, B Daan Westenbrink

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in Cardiovascular drugs and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Salva R YuristaDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.ORCID 0000-0001-9126-739X
Herman H W SilljéDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.
Kirsten T NijholtDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.
Martin M DokterDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.
Dirk J van VeldhuisenDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.
Rudolf A de BoerDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands.
B Daan WestenbrinkDepartment of Cardiology, University Medical Center Groningen, University of Groningen, PO Box 30.001, Groningen, 9700 RB, The Netherlands. b.d.westenbrink@umcg.nl.
University Medical Center Groningen · NL

Funding

Hartstichting CVON DOSIS, grant 2014-40, CVON SHE-PREDICTS-HF, grant 2017-21, and CVON RED-CVD, grant 2017-11Indonesia Endowment Fund for Education LPDP No. 20150722083422Nederlandse Organisatie voor Wetenschappelijk Onderzoek NWO VENI, grant 016.176.147Nederlandse Organisatie voor Wetenschappelijk Onderzoek NWO VIDI, grant 917.13.350
6 · The paper itself

Abstract

backgroundHeart failure (HF) is considered to be a prothrombotic condition and it has been suggested that coagulation factors contribute to maladaptive cardiac remodelling via activation of the protease-activated receptor 1 (PAR1). We tested the hypothesis that anticoagulation with the factor Xa (FXa) inhibitor apixaban would ameliorate cardiac remodelling in rats with HF after myocardial infarction (MI). METHODS AND

resultsMale Sprague-Dawley rats were either subjected to permanent ligation of the left ascending coronary artery (MI) or sham surgery. The MI and sham animals were randomly allocated to treatment with placebo or apixaban in the chow (150 mg/kg/day), starting 2 weeks after surgery. Cardiac function was assessed using echocardiography and histological and molecular markers of cardiac hypertrophy were assessed in the left ventricle (LV). Apixaban resulted in a fivefold increase in anti-FXa activity compared with vehicle, but no overt bleeding was observed and haematocrit levels remained similar in apixaban- and vehicle-treated groups. After 10 weeks of treatment, LV ejection fraction was 42 ± 3% in the MI group treated with apixaban and 37 ± 2 in the vehicle-treated MI group (p > 0.05). Both vehicle- and apixaban-treated MI groups also displayed similar degrees of LV dilatation, LV hypertrophy and interstitial fibrosis. Histological and molecular markers for pathological remodelling were also comparable between groups, as was the activity of signalling pathways downstream of the PAR1 receptor.

conclusionFXa inhibition with apixaban does not influence pathological cardiac remodelling after MI. These data do not support the use of FXa inhibitor in HF patients with the aim to amend the severity of HF. Graphical Abstract.

Indexed as

AnimalsElectrocardiographyFactor Xa InhibitorsHeart FailureHeart VentriclesHematocritHemorrhageHypertrophy, Left VentricularMaleMyocardial InfarctionPyrazolesPyridonesRandom AllocationRatsRats, Sprague-DawleyReceptor, PAR-1apixabanFactor Xa InhibitorsPyrazolesPyridonesReceptor, PAR-1AnticoagulantCardiac functionCardiac remodellingHeart failure

Identifiers

PMID32458320
PMCPMC8452585
OpenAlexW3029908925

What OpenQuestion holds

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Registered trials

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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.