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

GENomE wide analysis of sotalol-induced IKr inhibition during ventricular REPOLarization, "GENEREPOL study": Lack of common variants with large effect sizes.

PloS one - 1 Jan 2017

Salem Joe-Elie, Germain Marine, Hulot Jean-Sébastien, Voiriot Pascal, Lebourgeois Bruno, Waldura Jean, Tregouet David-Alexandre, Charbit Beny, Funck-Brentano Christian

Abstract excerpt

Many drugs used for non-cardiovascular and cardiovascular purposes, such as sotalol, have the side effect of prolonging cardiac repolarization, which can trigger life-threatening cardiac arrhythmias by inhibiting the potassium-channel IKr (KCNH2). On the electrocardiogram (ECG), IKr inhibition induces an increase in QTc and Tpeak-Tend (TpTe) interval and a decrease of T wave maximal amplitude (TAmp). These...

Read the complete abstract on PubMed

Topics

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

Share to Action Potentials
Share to Cohort Studies

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Demography

Share to Electrocardiography

Share to Heart Ventricles

Share to Potassium Channels

Share to Principal Component Analysis

Share to Reproducibility of Results

Source

Open in PubMed Open full text

Identifiers

PMID: 28800628
DOI: 10.1371/journal.pone.0181875
PMCID: PMC5553738

Genes

KCNH2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 1 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

GENomE wide analysis of sotalol-induced IKr inhibition during ventricular REPOLarization, "GENEREPOL study": Lack of common variants with large effect sizes.PMID 28800628Read ↗

A polygenic predictor of baseline QTc is associated with sotalol-induced QT prolongationSemantic proximity Read ↗

Modeling susceptibility to drug-induced long QT with a panel of subject-specific induced pluripotent stem cellsSemantic proximity Read ↗

Genome wide analysis of drug-induced torsades de pointes: lack of common variants with large effect sizes.Semantic proximity Read ↗

CAVIN1-Mediated Endocytosis: A Novel Mechanism Underlying The Interindividual Variability In Drug-Induced Long QTSemantic proximity Read ↗

T-wave morphology abnormalities in benign, potent, and arrhythmogenic I(kr) inhibition.Semantic proximity Read ↗

Blinded In Silico Drug Trial Reveals the Minimum Set of Ion Channels for Torsades de Pointes Risk AssessmentSemantic proximity Read ↗

A common polymorphism in KCNH2 (HERG) hastens cardiac repolarization.Semantic proximity Read ↗

Genetic determinants of QT interval variation and sudden cardiac death.Semantic proximity Read ↗

Impaired T-amplitude adaptation to heart rate characterizes I(Kr) inhibition in the congenital and acquired forms of the long QT syndrome.Semantic proximity Read ↗

Molecular predictors of drug-induced prolongation of the QT interval.Semantic proximity Read ↗

A meta-analysis of genome-wide association studies of the electrocardiographic early repolarization pattern.Semantic proximity Read ↗

The action of the novel gastrointestinal prokinetic prucalopride on the HERG K+ channel and the common T897 polymorph.Semantic proximity Read ↗

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