Drug-induced block of the cardiac rapid delayed rectifying potassium current (<i>I</i><sub>Kr</sub>), carried by the human ether-a-go-go-related gene (hERG) channel, is the most common cause of acquired long QT syndrome.
Cardiac potassium channels encoded by human ether-à-go-go-related gene (<i>hERG</i>) are major targets for structurally diverse drugs associated with acquired long QT syndrome.
Contribution of a KCNH2 variant in genotyped long QT syndrome: Romano-Ward syndrome under double mutations and acquired long QT syndrome under heterozygote.
These findings indicate that roxithromycin may cause acquired long-QT syndrome via direct inhibition of hERG current and by disruption of hERG protein trafficking.
Our findings suggest that KCR1 genetic variations that diminish the ability of KCR1 to protect KCNH2 from inhibition by commonly used therapeutic agents constitute a risk factor for the aLQTS.
Since blockade of cardiac human ether-a-go-go-related gene (hERG) channels is an important cause of acquired long QT syndrome, we investigated the acute effects of desipramine on hERG channels to determine the electrophysiological basis for its pro-arrhythmic potential.
Ion channels encoded by the human ether-a-go-go-related gene (HERG) give rise to the rapidly activating delayed rectifier K+ current (IKr), the perturbation of which causes ventricular arrhythmias associated with inherited and acquired long QT syndrome.
Since blockade of cardiac human ether-a-go-go-related gene (hERG) channels is an important cause of acquired long QT syndrome, we investigated the acute effects of clomipramine on hERG channels to determine the electrophysiological basis for its proarrhythmic potential.
DNA samples were screened for the four common Finnish founder mutations (KCNQ1 G589D and IVS7-2A-->G, HERGL552S, and R176W), which are known to account for the majority of inherited LQTS in Finland.
Unintended block of HERG K+ channels is a side effect of many common medications and is the most common cause of acquired long QT syndrome associated with increased risk of life-threatening arrhythmias.