Evidence map›Paper›PMID 40714045›Full record

ArticleJournal of molecular and cellular cardiology2025

Compromised repolarization reserve in a murine model of catecholaminergic polymorphic ventricular tachycardia caused by RyR2-R420Q mutation.

Spyros Zissimopoulos, Pavel Kirilenko, Aitana Braza-Boïls, Esther Zorio, Yueyi Wang, Ana Maria Gomez, Mark B Cannell, Branko Latinkic, Ewan D Fowler

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In one paragraph

Article in Journal of molecular and cellular cardiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

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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

2 citing papers in PubMed.

  1. Article
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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

9 authors.

Spyros ZissimopoulosInstitute of Life Science, Swansea University Medical School, Swansea University, Swansea SA2 8PP, UK.
Pavel KirilenkoSchool of Biosciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff CF10 3AX, UK.
Aitana Braza-BoïlsCAFAMUSME Research Group, Instituto de Investigación Sanitaria La Fe de Valencia, Spain; CIBERCV, Center for Biomedical Network Research on Cardiovascular Diseases, Madrid, Spain.
Esther ZorioCAFAMUSME Research Group, Instituto de Investigación Sanitaria La Fe de Valencia, Spain; CIBERCV, Center for Biomedical Network Research on Cardiovascular Diseases, Madrid, Spain; Inherited Cardiac Diseases Unit, Cardiology Department at the Hospital Universitario y Politécnico La Fe de Valencia, Spain; Department of Medicine, Faculty of Medicine and Dentistry, Universitat de València, 46010, Valencia, Spain.
Yueyi WangInserm, UMR-S 1180, Signalling and Cardiovascular Pathophysiology, Faculté de Pharmacie, Université Paris-Saclay, 17 Avenue des Sciences, 91400 Orsay, France.
Ana Maria GomezInserm, UMR-S 1180, Signalling and Cardiovascular Pathophysiology, Faculté de Pharmacie, Université Paris-Saclay, 17 Avenue des Sciences, 91400 Orsay, France.
Mark B CannellSchool of Physiology, Pharmacology & Neuroscience, Faculty of Biomedical Sciences, University of Bristol, University Walk, Bristol BS8 1TD, UK.
Branko LatinkicSchool of Biosciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff CF10 3AX, UK.
Ewan D FowlerSchool of Biosciences, College of Biomedical and Life Sciences, Cardiff University, Cardiff CF10 3AX, UK. Electronic address: FowlerED@Cardiff.ac.uk.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCatecholaminergic polymorphic ventricular tachycardia (CPVT) is a malignant inherited heart disease characterised by stress-induced arrhythmias that are thought to be caused by delayed afterdepolarizations resulting from abnormal Ca

methodsElectrocardiograms were recorded in patients with RyR2-R420Q CPVT mutation (R420Q). Experiments were performed on control and R420Q knock-in mouse hearts and ventricular myocytes.

resultsR420Q patients had larger resting U-waves than family member controls. R420Q mouse hearts exhibited greater prolongation of monophasic APs following pauses in pacing and during beta-adrenergic stimulation. Ventricular ectopic beats during repolarization were more prevalent in R420Q mouse hearts following pacing-pauses and during premature electrical stimulation. Early afterdepolarizations (EADs) occurred in isolated R420Q myocytes during beta-adrenergic stimulation and coincided with increased Ca

conclusionsCa

Indexed as

MutationRyanodine Receptor Calcium Release ChannelTachycardia, VentricularAction PotentialsAnimalsCalciumDisease Models, AnimalElectrocardiographyFemaleHumansMaleMiceMice, TransgenicMyocytes, CardiacPolymorphic Catecholaminergic Ventricular TachycardiaCalciumryanodine receptor 2. mouseRyanodine Receptor Calcium Release ChannelArrhythmiasCalcium sparksCPVTEarly afterdepolarizationsRepolarization reserve

Identifiers

PMID40714045
PMCPMC7619069

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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.