Evidence map›Paper›PMID 40536467›Full record

ArticleJACC. Basic to translational science2025

Controlled Right Ventricular Pressure Overload Can Rescue Left Ventricular Dysfunction by Promoting Biventricular Adaptive Hypertrophy.

Matteo Ponzoni, Azadeh Yeganeh, Libo Zhang, Jennifer Zhang, Ramesh B Vanama, Kaley Hogarth, Quynh N Phi, Jing Li, Loukmane Karim, John G Coles and 1 more

Abstract read
In one paragraph

Article in JACC. Basic to translational science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

11 authors.

Matteo PonzoniDivision of Cardiovascular Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada.
Azadeh YeganehProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Libo ZhangProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Jennifer ZhangProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Ramesh B VanamaProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Kaley HogarthProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Quynh N PhiProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Jing LiProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
Loukmane KarimProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada.
John G ColesDivision of Cardiovascular Surgery, The Hospital for Sick Children, Toronto, Ontario, Canada.
Jason T MaynesProgram in Molecular Medicine, SickKids Research Institute, Toronto, Ontario, Canada; Department of Anesthesia and Pain Medicine, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Anesthesiology and Pain Medicine, University of Toronto, Toronto, Ontario, Canada. Electronic address: jason.maynes@sickkids.ca.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pulmonary artery banding (PAB) has been investigated as a therapy for left ventricular (LV) dysfunction in pediatric dilated cardiomyopathy; however, the underlying mechanisms of action of PAB-induced LV rehabilitation remain unknown. This study aims to establish a small animal model of PAB-treated LV dysfunction to document the biventricular hemodynamic and tissue-level modifications promoted by PAB. Sprague-Dawley rats underwent left anterior descending (LAD) artery ligation (LV dysfunction model) followed by PAB 1-week post-injury (LAD + PAB, n = 13). Controls consisted of sham (n = 16), PAB-only (n = 16), and LAD rats (n = 15). The animals underwent weekly echocardiography and terminal histopathology 4 weeks after surgery. Data shown as mean ± SEM or median (Q1-Q3). LAD + PAB rats exhibited positive LV remodeling (LV end-diastolic volume: 0.49 ± 0.02 mL vs 0.66 ± 0.03 mL; P < 0.001), improvement of LV ejection fraction (0.48 ± 0.01 vs. 0.36 ± 0.01; P < 0.001), and normalization of mitral valve Doppler E/A (1.43 ± 0.03 vs 1.91 ± 0.09; P < 0.001) compared to LAD animals. Histologic analysis documented LV hypertrophy (wall thickness/body weight: 9.3 ± 0.4 μm/g vs 7.2 ± 0.3 μm/g; P = 0.005), increased LV cardiomyocyte diameter (14.8 [Q1-Q3: 13.9-15.7] μm vs 11.3 [Q1-Q3: 10.8-11.7] μm; P = 0.001), and augmented neoangiogenesis (6.5 ± 0.2 vessels/mm

Indexed as

dilated cardiomyopathyexperimental modelleft ventricular dysfunctionpulmonary artery banding

Identifiers

PMID40536467
PMCPMC12399129

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.