[Inherited cardiac diseases caused by Nav1.5 sodium channel mutations]

Ugeskr Laeger. 2009 Apr 6;171(15):1261-5.
[Article in Danish]

Abstract

Contraction of the heart is achieved through a delicately regulated conduction of electrical impulses. A pivotal element in the impulse propagation is the depolarising sodium current responsible for the initial depolarisation of the cardiomyocytes. Recent research has shown that mutations in the gene encoding the cardiac sodium channel (SCN5A) is associated with both rare forms of ventricular arrhythmia, and with the most frequent form of arrhythmia, atrial fibrillation.

Publication types

  • English Abstract
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Atrial Fibrillation / genetics*
  • Atrial Fibrillation / physiopathology
  • Brugada Syndrome / genetics*
  • Brugada Syndrome / physiopathology
  • Heart Conduction System / physiopathology
  • Humans
  • Long QT Syndrome / genetics*
  • Long QT Syndrome / physiopathology
  • Muscle Proteins / genetics*
  • Mutation
  • NAV1.5 Voltage-Gated Sodium Channel
  • Sodium Channels / genetics*

Substances

  • Muscle Proteins
  • NAV1.5 Voltage-Gated Sodium Channel
  • SCN5A protein, human
  • Sodium Channels