Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Antiarrhythmic Action of Flecainide in Polymorphic Ventricular Arrhythmias Caused by a Gain-of-Function Mutation in the Nav 1.5 Sodium Channel.

Annals of noninvasive electrocardiology : the official journal of the International Society for Holter and Noninvasive Electrocardiology, Inc - 1 Jul 2016

Amarouch Mohamed Y, Swan Heikki, Leinonen Jaakko, Marjamaa Annukka, Lahtinen Annukka M, Kontula Kimmo, Toivonen Lauri, Widen Elisabeth, Abriel Hugues

Abstract excerpt

BACKGROUND: The cardiac sodium channel Nav 1.5, encoded by the gene SCN5A, is associated with a wide spectrum of hereditary arrhythmias. The gain-of-function mutation p.I141V in SCN5A was identified in a large multigenerational family with exercise-induced polymorphic ventricular arrhythmias. The purpose of this study was to evaluate the molecular and clinical effects of flecainide administration on patients with...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Aged
Share to Anti-Arrhythmia Agents

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Electrocardiography

Share to Exercise Test

Share to Flecainide

Share to HEK293 Cells

Share to NAV1.5 Voltage-Gated Sodium Channel

Share to Patch-Clamp Techniques

Source

Open in PubMed Open full text

Identifiers

PMID: 26965448
DOI: 10.1111/anec.12312
PMCID: PMC6931835

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 4 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Antiarrhythmic Action of Flecainide in Polymorphic Ventricular Arrhythmias Caused by a Gain-of-Function Mutation in the Nav 1.5 Sodium Channel.PMID 26965448Read ↗

Gain-of-function mutation of the SCN5A gene causes exercise-induced polymorphic ventricular arrhythmias.Semantic proximity Read ↗

Familial atrial fibrillation mutation M1875T-SCN5A increases early sodium current and dampens the effect of flecainide.Semantic proximity Read ↗

Gain-of-function mutation in SCN5A causes ventricular arrhythmias and early onset atrial fibrillationSemantic proximity Read ↗

Increased early sodium current causes familial atrial fibrillation and dampens effect of flecainideSemantic proximity Read ↗

Effects of flecainide in patients with new SCN5A mutation: mutation-specific therapy for long-QT syndrome?Semantic proximity Read ↗

The G213D variant in Nav1.5 alters sodium current and causes an arrhythmogenic phenotype resulting in a multifocal ectopic Purkinje-related premature contraction phenotype in human-induced pluripotent stem cell-derived cardiomyocytes.Semantic proximity Read ↗

Channel openings are necessary but not sufficient for use-dependent block of cardiac Na(+) channels by flecainide: evidence from the analysis of disease-linked mutations.Semantic proximity Read ↗

Flecainide Reduces Ventricular Arrhythmias in Patients With Genotype RyR2-positive Catecholaminergic Polymorphic Ventricular Tachycardia.Semantic proximity Read ↗

A common SCN5A variant alters the responsiveness of human sodium channels to class I antiarrhythmic agents.Semantic proximity Read ↗

In vivo studies of Scn5a+/- mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities.Semantic proximity Read ↗

Flecainide, a therapeutic option in a patient with long QT syndrome type 3 caused by the heterozygous V411M mutation in the SCN5A gene.Semantic proximity Read ↗

Mutations in the Kv1.5 channel gene KCNA5 in cardiac arrest patients.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.