ArticleActa physiologica (Oxford, England)2014
Arrhythmic substrate, slowed propagation and increased dispersion in conduction direction in the right ventricular outflow tract of murine Scn5a+/- hearts.
Article in Acta physiologica (Oxford, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 21 citations in OpenAlex.
- Atrial arrhythmogenesis and electrophysiological remodeling in hypokalaemic metabolic syndrome: the role of apamin-sensitive SK channels.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2025Article
- Electrical and Structural Insights into Right Ventricular Outflow Tract Arrhythmogenesis.International journal of molecular sciences · 2023Review
- NovelExperimental and therapeutic medicine · 2023Article
- Heterogeneities in Ventricular Conduction Following Treatment with Heptanol: A Multi-Electrode Array Study in Langendorff-Perfused Mouse Hearts.Life (Basel, Switzerland) · 2022Article
- Brugada Syndrome: Different Experimental Models and the Role of Human Cardiomyocytes From Induced Pluripotent Stem Cells.Journal of the American Heart Association · 2022Review
- Mechanisms of Arrhythmias in the Brugada Syndrome.International journal of molecular sciences · 2020Review
- Brugada Syndrome: Oligogenic or Mendelian Disease?International journal of molecular sciences · 2020Review
- Experimental Models of Brugada syndrome.International journal of molecular sciences · 2019Review
- Pretreatment with neuregulin-1 improves cardiac electrophysiological properties in a rat model of myocardial infarction.Experimental and therapeutic medicine · 2019Article
- Calcium in Brugada Syndrome: Questions for Future Research.Frontiers in physiology · 2018Review
- Murine Electrophysiological Models of Cardiac Arrhythmogenesis.Physiological reviews · 2017Review
- Electrophysiological characterization of a large set of novel variants in the SCN5A-gene: identification of novel LQTS3 and BrS mutations.Pflugers Archiv : European journal of physiology · 2016Article
- Fibrosis, Connexin-43, and Conduction Abnormalities in the Brugada Syndrome.Journal of the American College of Cardiology · 2015Article
- Flecainide exerts paradoxical effects on sodium currents and atrial arrhythmia in murine RyR2-P2328S hearts.Acta physiologica (Oxford, England) · 2015Article
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Authors and funding
9 authors at 4 institutions in 6 countries.
Funding
Abstract
aimTo test a hypothesis attributing arrhythmia in Brugada Syndrome to right ventricular (RV) outflow tract (RVOT) conduction abnormalities arising from Nav 1.5 insufficiency and fibrotic change.
methodsArrhythmic properties of Langendorff-perfused Scn5a+/- and wild-type mouse hearts were correlated with ventricular effective refractory periods (VERPs), multi-electrode array (MEA) measurements of action potential (AP) conduction velocities and dispersions in conduction direction (CD), Nav 1.5 expression levels, and fibrotic change, as measured at the RVOT and RV. Two-way anova was used to test for both independent and interacting effects of anatomical region and genotype on these parameters.
resultsScn5a+/- hearts showed greater arrhythmic frequencies during programmed electrical stimulation at the RVOT but not the RV. The Scn5a+/- genotype caused an independent increase of VERP regardless of whether the recording site was the RVOT or RV. Effective AP conduction velocities (CV†s), derived from fitting regression planes to arrays of observed local activation times were reduced in Scn5a+/- hearts and at the RVOT independently. AP conduction velocity magnitudes derived by averaging MEA results from local vector analyses, CV*, were reduced by the Scn5a+/- genotype alone. In contrast, dispersions in conduction direction, were greater in the RVOT than the RV, when the atrioventricular node was used as the pacing site. The observed reductions in Nav 1.5 expression were attributable to Scn5a+/-, whereas increased levels of fibrosis were associated with the RVOT.
conclusionsThe Scn5a+/- RVOT recapitulates clinical findings of increased arrhythmogenicity through reduced CV† reflecting reduced CV* attributable to reduced Nav 1.5 expression and increased CD attributable to fibrosis.
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