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Renal denervation for treating congenital long QT syndrome: shortening the QT interval or modulating sympathetic tone?

08:00 EDT 11th October 2019 | BioPortfolio

Summary of "Renal denervation for treating congenital long QT syndrome: shortening the QT interval or modulating sympathetic tone?"

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Name: Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology
ISSN: 1532-2092
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Renal denervation for treating congenital long QT syndrome: shortening the QT interval or modulating sympathetic tone?-Author's reply.

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Medical and Biotech [MESH] Definitions

A form of ventricular pre-excitation characterized by a short PR interval and a long QRS interval with a delta wave. In this syndrome, atrial impulse conducts to the HEART VENTRICLES via an accessory pathway located between the wall of the right or left atria and the ventricles, known as the bundle of Kent. The inherited form can be caused by mutation of PRKAG2 gene encoding a gamma-2 regulatory subunit of AMP-activated protein kinase.

A condition that is characterized by episodes of fainting (SYNCOPE) and varying degree of ventricular arrhythmia as indicated by the prolonged QT interval. The inherited forms are caused by mutation of genes encoding cardiac ion channel proteins. The two major forms are ROMANO-WARD SYNDROME and JERVELL-LANGE NIELSEN SYNDROME.

A form of ventricular pre-excitation characterized by a normal PR interval and a long QRS interval with an initial slow deflection (delta wave). In this syndrome, the atrial impulse travel to the ventricle via the Mahaim fibers which connect ATRIOVENTRICULAR NODE directly to the right ventricle wall (nodoventricular pathway) or to the RIGHT BUNDLE BRANCH OF HIS (nodofascicular pathway).

A form of long QT syndrome that is without congenital deafness. It is caused by mutation of the KCNQ1 gene which encodes a protein in the VOLTAGE-GATED POTASSIUM CHANNEL.

A sex-linked recessive disorder affecting multiple systems including the EYE, the NERVOUS SYSTEM, and the KIDNEY. Clinical features include congenital CATARACT; MENTAL RETARDATION; and renal tubular dysfunction (FANCONI SYNDROME; RENAL TUBULAR ACIDOSIS; X-LINKED HYPOPHOSPHATEMIA or vitamin-D-resistant rickets) and SCOLIOSIS. This condition is due to a deficiency of phosphatidylinositol 4,5-bisphosphate-5-phosphatase leading to defects in PHOSPHATIDYLINOSITOL metabolism and INOSITOL signaling pathway. (from Menkes, Textbook of Child Neurology, 5th ed, p60; Am J Hum Genet 1997 Jun;60(6):1384-8)

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