[Genetic background predisposing the drug-induced long QT syndrome]

Nihon Yakurigaku Zasshi. 2003 Jun;121(6):401-7. doi: 10.1254/fpj.121.401.
[Article in Japanese]

Abstract

Molecular and cellular mechanisms underlying the QT prolongation have been elucidated largely because of the recent understanding of the generation of the congenital forms of QT prolongation; i.e., the long QT syndrome. To date, at least 7 different genes that modulate cardiac ion channels were identitied to be associated with the syndrome. In the clinical setting, the drug-induced long QT syndrome is more frequently seen and therefore important. We found several mutations as well as an SNP specific among the Japanese population in probands referred to as the secondary long QT patients, including the drug-induced cases. These findings raised the potential that there are also predisposing risk factors at patient's side.

Publication types

  • Review

MeSH terms

  • Cation Transport Proteins*
  • DNA-Binding Proteins*
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • Genetic Predisposition to Disease
  • Humans
  • KCNQ Potassium Channels
  • KCNQ1 Potassium Channel
  • Long QT Syndrome / chemically induced
  • Long QT Syndrome / genetics*
  • Mutation
  • NAV1.5 Voltage-Gated Sodium Channel
  • Polymorphism, Single Nucleotide
  • Potassium Channels / genetics
  • Potassium Channels, Voltage-Gated*
  • Sodium Channels / genetics
  • Torsades de Pointes / genetics
  • Trans-Activators*
  • Transcriptional Regulator ERG

Substances

  • Cation Transport Proteins
  • DNA-Binding Proteins
  • ERG protein, human
  • ERG1 Potassium Channel
  • Ether-A-Go-Go Potassium Channels
  • KCNH6 protein, human
  • KCNQ Potassium Channels
  • KCNQ1 Potassium Channel
  • KCNQ1 protein, human
  • NAV1.5 Voltage-Gated Sodium Channel
  • Potassium Channels
  • Potassium Channels, Voltage-Gated
  • SCN5A protein, human
  • Sodium Channels
  • Trans-Activators
  • Transcriptional Regulator ERG