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

Beneficial normalization of cardiac repolarization by carnitine in transgenic short QT syndrome type 1 rabbit models.

Cardiovascular research - 5 Nov 2024

Bodi Ilona, Mettke Lea, Michaelides Konstantin, Hornyik Tibor, Meier Stefan, Nimani Saranda, Perez-Feliz Stefanie, El-Battrawy Ibrahim, Bugger Heiko, Zehender Manfred, Brunner Michael, Heijman Jordi, Odening Katja E

Abstract excerpt

AIMS: Short QT syndrome type 1 (SQT1) is a genetic channelopathy caused by gain-of-function variants in human-ether-a-go-go (HERG) underlying the rapid delayed-rectifier K+ current (IKr), leading to QT-shortening, ventricular arrhythmias, and sudden cardiac death. Data on efficient pharmacotherapy for SQT1 are scarce. In patients with primary carnitine-deficiency, acquired-short QT syndrome (SQTS) has been...

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 Arrhythmias, Cardiac

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Carnitine

Share to ERG1 Potassium Channel

Share to Heart Conduction System

Share to Heart Rate

Share to Models, Cardiovascular

Share to Tachycardia, Ventricular

Source

Open in PubMed Open full text

Identifiers

PMID: 39018021
DOI: 10.1093/cvr/cvae149
PMCID: PMC11535723

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Beneficial normalization of cardiac repolarization by carnitine in transgenic short QT syndrome type 1 rabbit models.PMID 39018021Read ↗

A novel transgenic rabbit model with reduced repolarization reserve: long QT syndrome caused by a dominant-negative mutation of the KCNE1 gene.Semantic proximity Read ↗

In silico investigation of a KCNQ1 mutation associated with short QT syndrome.Semantic proximity Read ↗

Preclinical short QT syndrome models: studying the phenotype and drug-screening.Semantic proximity Read ↗

Proarrhythmia in KCNJ2-linked short QT syndrome: insights from modelling.Semantic proximity Read ↗

Increased vulnerability of human ventricle to re-entrant excitation in hERG-linked variant 1 short QT syndrome.Semantic proximity Read ↗

Repurposing polyamines to prevent arrhythmias in Short QT Syndrome type 3, a potentially lethal diseaseSemantic proximity Read ↗

In silico assessment of the effects of quinidine, disopyramide and E-4031 on short QT syndrome variant 1 in the human ventricles.Semantic proximity Read ↗

Repurposing polyamines to prevent life-threatening arrhythmias in Short QT Syndrome type 3.Semantic proximity Read ↗

Docosahexaenoic acid normalizes QT interval in long QT type 2 transgenic rabbit models in a genotype-specific fashion.Semantic proximity Read ↗

A novel computational model of swine ventricular myocyte reveals new insights into disease mechanisms and therapeutic approaches in Timothy Syndrome.Semantic proximity Read ↗

Differential conditions for early after-depolarizations and triggered activity in cardiomyocytes derived from transgenic LQT1 and LQT2 rabbits.Semantic proximity Read ↗

Computational analysis of arrhythmogenesis in KCNH2 T618I mutation-associated short QT syndrome and the pharmacological effects of quinidine and sotalol.Semantic proximity Read ↗

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