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Article

Normal interventricular differences in tissue architecture underlie right ventricular susceptibility to conduction abnormalities in a mouse model of Brugada syndrome.

Cardiovascular research - 1 Apr 2018

Kelly Allen, Salerno Simona, Connolly Adam, Bishop Martin, Charpentier Flavien, Stølen Tomas, Smith Godfrey L

Abstract excerpt

Aims: Loss-of-function of the cardiac sodium channel NaV1.5 is a common feature of Brugada syndrome. Arrhythmias arise preferentially from the right ventricle (RV) despite equivalent NaV1.5 downregulation in the left ventricle (LV). The reasons for increased RV sensitivity to NaV1.5 loss-of-funct...

Topics

Action Potentials
Animals
Brugada Syndrome
Disease Models, Animal
Genetic Predisposition to Disease
Heart Rate
Heart Ventricles
Mice, 129 Strain
Mice, Knockout
Microscopy, Fluorescence, Multiphoton
NAV1.5 Voltage-Gated Sodium Channel

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Phenotype

Time Factors

Ventricular Function, Left

Ventricular Function, Right

Voltage-Sensitive Dye Imaging

Source

Open in PubMed Open full text

Identifiers

PMID: 29267949
DOI: 10.1093/cvr/cvx244
PMCID: PMC5915948

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 30 Aug 2026. Prepared record publication-29267949-2026-08-30.1. Manifest publication-graph-cohort-2026-08-30.1.

Source receipt: PubMed via Helena Literature Corpus, retrieved 30 Aug 2026.

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