Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
We identified the KCNH2-H562R mutation in a 65-year-old man with a prolonged QTc interval who had experienced an episode of torsade de pointes.
|
25819988 |
2015 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
We describe a case of torsade de pointes (TdP) caused by sevoflurane in a patient with c-LQTS genotype 2 (LQT2).
|
27555138 |
2016 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
LHGDN |
To determine what role genetic variation in the hERG gene plays in drug-induced arrhythmias, we screened DNA samples collected from 105 atrial-fibrillation patients treated with dofetilide for polymorphisms, seven of whom developed TdP.
|
15522280 |
2004 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Thus, patients with an acute MI carrying the KCNH2-K897T polymorphism had an 8-fold greater risk of experiencing TdP compared with controls (95% confidence interval = 2-40).
|
22338672 |
2012 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
This study evaluated the I Kr blocking potency of a series of antiarrhythmics associated with a range of clinical risks of TdP in two such systems: mouse AT-1 cells (in which I Kr is the major repolarizing current) and Ltk cells transiently transfected with HERG (n = 4-10 cells per drug).
|
11602820 |
2001 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
These data indicate that HERG is LQT2 and suggest a likely cellular mechanism for torsade de pointes.
|
7889573 |
1995 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The most common problem is acquired long QT syndrome caused by drugs that block human ether-a-go-go-related-gene (hERG) K(+) channels, delay cardiac repolarization and increase the risk of torsades de pointes arrhythmia (TdP).
|
15749156 |
2005 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
The main mechanism underlying an acquired QT syndrome and a potentially fatal arrhythmia called torsades de pointes is the inhibition of potassium channel encoded by hERG (the human ether-a-go-go-related gene).
|
18988205 |
2009 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The main mechanism of QT prolongation and TdP is block of the rapid component of the cardiac delayed rectifier K(+) current (I(Kr)), which is encoded by hERG (human ether-à-go-go-related gene).
|
20467834 |
2010 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The level of inhibition of the human Ether-à-go-go-related gene (hERG) channel is one of the earliest preclinical markers used to predict the risk of a compound causing Torsade-de-Pointes (TdP) arrhythmias.
|
21300721 |
2011 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The blockade of the human ether-a-go-go-related gene (HERG) channel is a major concern for QT prolongation and Torsade de Pointes risk.
|
23103500 |
2013 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
The antihistamine terfenadine blocks HERG channels, and can cause QT prolongation and torsades de pointes, whereas its carboxylate fexofenadine lacks HERG blocking activity.2.
|
12411421 |
2002 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Role of a KCNH2 polymorphism (R1047 L) in dofetilide-induced Torsades de Pointes.
|
15522280 |
2004 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Rare mutations in KCNH2 provide the pathogenic substrate for type 2 congenital long QT syndrome (LQTS), thus placing this cardiac potassium channel squarely in the intersection between congenital LQTS (the "Rosetta stone" of the heritable channelopathies) and acquired LQTS (drug-induced TdP).
|
16253929 |
2005 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
Putative interactions between the Human Ether-a-go-go Related Gene (HERG), QT interval prolongation and Torsades de Pointes (TdP) are now integral components of any discussion on drug safety.
|
15464027 |
2004 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
Propranolol (1 micromol/L), a beta blocker, completely prevented the effect of isoproterenol to persistently or transiently increase TDR and to induce TdP in the LQT1 and LQT2 models, but facilitated TdP in the LQT3 model.
|
10688323 |
1999 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
CTD_human |
Probucol aggravates long QT syndrome associated with a novel missense mutation M124T in the N-terminus of HERG.
|
15043509 |
2004 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
Pause dependence of TdP onset is predominant in LQT2 but absent or rare in LQT1.
|
17088455 |
2006 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
CTD_human |
Mechanisms of arsenic-induced prolongation of cardiac repolarization.
|
15213294 |
2004 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
KCNQ1 and KCNH2 are the two most common potassium channel genes causing long QT syndrome (LQTS), an inherited cardiac arrhythmia featured by QT prolongation and increased risks of developing torsade de pointes and sudden death.
|
18808722 |
2008 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
In LQTS2, an aberrant HERG gene that encodes the potassium channel IKr leads to insufficient IKr activity and delayed repolarization, causing ECG abnormalities and torsades de pointes (TdP).
|
10090227 |
1999 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
In long QT syndrome type 2 (I<sub>Kr</sub> blockade or bradycardia), the higher Ca<sup>2+</sup> influx via I<sub>Ca,L</sub> causes Ca<sup>2+</sup> overload, spontaneous sarcoplasmic reticulum Ca<sup>2+</sup> release, and reactivation of I<sub>Ca,L</sub> that triggers early afterdepolarizations and torsades de pointes.
|
29330129 |
2018 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
However, typical cases of Torsade de pointes occurred in association with AV block and LQT2.
|
29929706 |
2018 |
Torsades de Pointes
|
0.500 |
GeneticVariation
|
disease |
BEFREE |
High concentrations of intravenous nicorandil, a potassium channel opener, have been shown to be capable of decreasing QT and TDR, and preventing TdP in LQT1 and LQT2 but not in LQT3.
|
15892662 |
2005 |
Torsades de Pointes
|
0.500 |
Biomarker
|
disease |
BEFREE |
Her ECG revealed QT-prolongation associated with LQT2-specific T-U wave patterns, T wave alternans, long QT-dependent torsade de pointes (TdP) and ventricular fibrillation (VF).
|
29037423 |
2019 |