Long QT syndrome 2

Common Name(s)

Long QT syndrome 2

Congenital long QT syndrome is electrocardiographically characterized by a prolonged QT interval and polymorphic ventricular arrhythmias (torsade de pointes). These cardiac arrhythmias may result in recurrent syncope, seizure, or sudden death ({7:Jongbloed et al., 1999}). For a discussion of genetic heterogeneity of long QT syndrome, see LQT1 ({192500}).
 

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Advocacy and Support Organizations

 

Condition Specific Organizations

Following organizations serve the condition "Long QT syndrome 2" for support, advocacy or research.

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General Support Organizations

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Scientific Literature

Articles from the PubMed Database

Research articles describe the outcome of a single study. They are the published results of original research.
The terms "Long QT syndrome 2" returned 34 free, full-text research articles on human participants. First 3 results:

Large-scale mutational analysis of Kv11.1 reveals molecular insights into type 2 long QT syndrome.
 

Author(s): Corey L Anderson, Catherine E Kuzmicki, Ryan R Childs, Caleb J Hintz, Brian P Delisle, Craig T January

Journal:

 

It has been suggested that deficient protein trafficking to the cell membrane is the dominant mechanism associated with type 2 Long QT syndrome (LQT2) caused by Kv11.1 potassium channel missense mutations, and that for many mutations the trafficking defect can be corrected pharmacologically. ...

Last Updated: 24 Nov 2014

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Calmodulin mutations associated with long QT syndrome prevent inactivation of cardiac L-type Ca(2+) currents and promote proarrhythmic behavior in ventricular myocytes.
 

Author(s): Worawan B Limpitikul, Ivy E Dick, Rosy Joshi-Mukherjee, Michael T Overgaard, Alfred L George, David T Yue

Journal: J. Mol. Cell. Cardiol.. 2014 Sep;74():115-24.

 

Recent work has identified missense mutations in calmodulin (CaM) that are associated with severe early-onset long-QT syndrome (LQTS), leading to the proposition that altered CaM function may contribute to the molecular etiology of this subset of LQTS. To date, however, no experimental ...

Last Updated: 28 Jul 2014

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Re-trafficking of hERG reverses long QT syndrome 2 phenotype in human iPS-derived cardiomyocytes.
 

Author(s): Ashish Mehta, Glen Lester Sequiera, Chrishan J A Ramachandra, Yuliansa Sudibyo, Yingying Chung, Jingwei Sheng, Keng Yean Wong, Teng Hong Tan, Philip Wong, Reginald Liew, Winston Shim

Journal: Cardiovasc. Res.. 2014 Jun;102(3):497-506.

 

Long QT syndrome 2 (LQTS2) caused by missense mutations in hERG channel is clinically associated with abnormally prolonged ventricular repolarization and sudden cardiac deaths. Modelling monogenic arrhythmogenic diseases using human-induced pluripotent stem cells (hiPSCs) offers unprecedented ...

Last Updated: 23 May 2014

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Reviews from the PubMed Database

Review articles summarize what is currently known about a disease. They discuss research previously published by others.
The terms "Long QT syndrome 2" returned 0 free, full-text review articles on human participants.

 
 
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Clinical Trial Information This information is provided by ClinicalTrials.gov

Effect of GS-6615 on QT, Safety, and Tolerability in Adults With Long QT2 Syndrome
 

Status: Recruiting

Condition Summary: LQT2 Syndrome

 

Last Updated: 20 Jan 2016

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Comparison Between Epinephrine and Exercise Test in QT Long Syndrome Patients
 

Status: Recruiting

Condition Summary: Long QT Syndrome Type 1 or 2

 

Last Updated: 23 May 2014

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Fat and Sugar Metabolism During Exercise in Patients With Metabolic Myopathy
 

Status: Not yet recruiting

Condition Summary: Metabolism, Inborn Errors; Lipid Metabolism, Inborn Errors; Carbohydrate Metabolism, Inborn Errors; Long-Chain 3-Hydroxyacyl-CoA Dehydrogenase Deficiency; Glycogenin-1 Deficiency (Glycogen Storage Disease Type XV); Carnitine Palmitoyl Transferase 2 Deficiency; VLCAD Deficiency; Medium-chain Acyl-CoA Dehydrogenase Deficiency; Multiple Acyl-CoA Dehydrogenase Deficiency; Carnitine Transporter Deficiency; Neutral Lipid Storage Disease; Glycogen Storage Disease Type II; Glycogen Storage Disease Type III; Glycogen Storage Disease Type IV; Glycogen Storage Disease Type V; Muscle Phosphofructokinase Deficiency; Phosphoglucomutase 1 Deficiency; Phosphoglycerate Mutase Deficiency; Phosphoglycerate Kinase Deficiency; Phosphorylase Kinase Deficiency; Beta Enolase Deficiency; Lactate Dehydrogenase Deficiency; Glycogen Synthase Deficiency

 

Last Updated: 15 Dec 2015

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