Evidence map›Paper›PMID 28985746›Full record

ArticleJournal of translational medicine2017

Porcine model of progressive cardiac hypertrophy and fibrosis with secondary postcapillary pulmonary hypertension.

Mariann Gyöngyösi, Noemi Pavo, Dominika Lukovic, Katrin Zlabinger, Andreas Spannbauer, Denise Traxler, Georg Goliasch, Ljubica Mandic, Jutta Bergler-Klein, Alfred Gugerell and 10 more

Open access · goldAbstract read
In one paragraph

Article in Journal of translational medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 40 citations in OpenAlex.

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  4. Sexual dimorphism in animal models of heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2025
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  14. Animal models of pulmonary hypertension due to left heart disease.Animal models and experimental medicine · 2022
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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 4 institutions in 3 countries.

Mariann GyöngyösiDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria. mariann.gyongyosi@meduniwien.ac.at.
Noemi PavoDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Dominika LukovicDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Katrin ZlabingerDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Andreas SpannbauerDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Denise TraxlerDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Georg GoliaschDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Ljubica MandicDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Jutta Bergler-KleinDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Alfred GugerellDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Andras JakabDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Zsuzsanna SzankaiDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Levente TothInstitute of Diagnostic Imaging and Radiation Oncology, University of Kaposvar, Kaposvar, Hungary.
Rita GaramvölgyiInstitute of Diagnostic Imaging and Radiation Oncology, University of Kaposvar, Kaposvar, Hungary.
Gerald MaurerDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Frederic JaisserINSERM, UMRS 1138, Team 1, Centre de Recherche des Cordeliers, Pierre et Marie Curie University, Paris Descartes University, Paris, France.
Faiez ZannadCentre d'Investigation Clinique Inserm, CHU, Université de Lorraine, Nancy, France.
Thomas ThumInstitute for Molecular and Translational Therapeutic Strategies (IMTTS), Hannover, Germany.
Sándor BátkaiInstitute for Molecular and Translational Therapeutic Strategies (IMTTS), Hannover, Germany.
Johannes WinklerDepartment of Cardiology, Medical University of Vienna, Währinger Gürtel 18-20, 1090, Vienna, Austria.
Medical University of Vienna · ATUniversity of Kapsovar · HUCentre de Recherche des Cordeliers · FRUniversité de Lorraine · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMeaningful translational large animal models for cardiac diseases are indispensable for studying disease mechanisms, development of novel therapeutic strategies, and evaluation of potential drugs.

methodsFor induction of heart failure, cardiac hypertrophy and fibrosis, a bare metal stent was implanted in the descending aorta of growing pigs (n = 7), inducing pressure stress on the left ventricle (group HYPI). The constant stent size in growing pigs resulted in antegrade partial obstruction of the aortic flow with a gradual increase in afterload. Five pigs with sham intervention served as control. Serial haemodynamic, pressure-volume loop measurements and transthoracic echocardiography (TTE) were performed to detect developing pressure overload of the LV and cardiac MRI with late enhancement for measuring LV and RV mass and ejection fraction.

resultsAt 5-month follow-up, CT and contrast aortography, and intraluminal echocardiography confirmed aortic isthmus stenosis with a mean trans-stenotic gradient of 64 ± 13.9 mmHg. Invasive haemodynamic measurements revealed a secondary increase in pulmonary artery pressure (44.6 ± 5.1 vs 25.9 ± 6.2 mmHg, HYPI vs control, p < 0.05). TTE and ex vivo analyses confirmed severe concentric LV hypertrophy (mean circumferential wall thickness, 19.4 ± 3.1, n = 7 vs 11.4 ± 1.0 mm, n = 5, HYPI vs controls, p < 0.05). The LV and RV mass increased significantly, paralleled by increased isovolumic relaxation constant (tau). Histological analyses confirmed substantial fibrosis and myocyte hypertrophy in both LV and RV. Expressions of ANP, BNP, and miRNA-29a were up-regulated, while SERCA2a and miRNA-1 were down-regulated. Plasma NGAL levels increased gradually, while the elevation of NT-proBNP was detected only at the 5-month FUP.

conclusionThese data prove that percutaneous artificial aortic stenosis in pigs is useful for inducing clinically relevant progredient heart failure based on myocardial hypertrophy and fibrosis.

Indexed as

Disease ProgressionAnimalsAortic Valve StenosisBiomarkersCapillariesCardiomegalyDiastoleDisease Models, AnimalFibrosisGene Expression Regulation, NeoplasticHeart VentriclesHypertension, PulmonaryMagnetic Resonance Imaging, CineMaleMyocardiumPressureBiomarkersAortic isthmus stenosisCardiac hypertrophyGene expressionPET-MRI imagingTranslational large animal model

Identifiers

PMID28985746
PMCPMC5639584
OpenAlexW2761290171

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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.