KCNQ1

(redirected from LQT)
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KCNQ1

A gene on chromosome 11p15.5 that encodes a voltage-gated potassium channel required for the repolarisation phase of the cardiac action potential. The KCNQ1 gene product can form heteromultimers with two other potassium channel proteins, KCNE1 and KCNE3.
 
Molecular pathology
KCNQ1 mutations are associated with hereditary long QT syndrome/Romano-Ward syndrome, Jervell and Lange-Nielsen syndrome and familial atrial fibrillation.
References in periodicals archive ?
Nowadays, beta blockers as well as implantable cardioverter-defibrillators or cardiostimulators are used to treat LQT syndrome.
iPSC-derived cardiomyocytes to model LQT syndrome were firstly obtained in 2010.
In USA, congenital LQTS accounts for 3000 to 4000 sudden deaths in children annually.
T-wave abnormalities characteristic of LQTS may be: wide-based, slowly generated T; wide-based, double-hump, notched T; low amplitude deflection on the descending limb indistinct termination of T-wave (T-U complex); sinusoidal, slowly generated T-wave; or T-wave inscribed after prolonged ST segment.
An NN was proposed as a vehicle for the capturing of LQT data in off-the-shelf control systems, providing a straightforward framework for implementation, as shown in Rieger and Naidu (2005).
The mainstay of therapy in patients with LQTS remains beta-blockers, particularly in LQT1 patients.
Hereditary LQTS classically affects family members in multiple generations, reflecting an autosomal dominant pattern of inheritance.
LQTS can be either inherited or acquired and is associated with malignant ventricular arrhythmias, classically torsades de pointes (TdP).
Acquired LQTS reflects conditions under which a number of heterogeneous causative factors including drugs, metabolic disturbances (particularly hypokalemia and hypomagnesemia), or acute illness, lead to abnormal cardiac channel fluxes and prolonged repolarization.
LQTs Fire and Safety units former release of work consist of refurbishment, upgrades, and installation of all fire and gas analysis systems, foam suppression systems, and safety gears all over a drilling rig.
Furthermore, patients with low--or nonpenetrant genetic LQTS (16,17) may become symptomatic only when taking drugs prolonging the Q-T interval (18).
In the latter case, acquired LQTS may be seen after the use of a variety of medications (eg, antiarrhythmic medications, antihistamines, psychotropic drugs, antifungal drugs, or macrolide antibiotics) or with electrolyte abnormalities, such as hypokalemia.