Long QT syndrome

Cardiol Clin. 2000 May;18(2):309-25. doi: 10.1016/s0733-8651(05)70143-0.

Abstract

In conclusion, much has been learned in the past several years regarding the molecular biology of LQTS, and this information has been directly applicable to the clinical care of patients with this syndrome. The knowledge also has been of considerable importance for understanding the molecular basis of arrhythmias in general and is providing insights into potential molecular-based therapies for arrhythmias.

Publication types

  • Review

MeSH terms

  • Adrenergic beta-Antagonists / therapeutic use*
  • Cation Transport Proteins*
  • DNA-Binding Proteins*
  • Death, Sudden, Cardiac / prevention & control
  • Diagnosis, Differential
  • ERG1 Potassium Channel
  • Electrocardiography
  • Enzyme Inhibitors / therapeutic use
  • Ether-A-Go-Go Potassium Channels
  • Genetic Predisposition to Disease
  • Genotype
  • Humans
  • Ion Channels / antagonists & inhibitors
  • Ion Channels / genetics
  • Ion Channels / metabolism
  • Long QT Syndrome* / diagnosis
  • Long QT Syndrome* / genetics
  • Long QT Syndrome* / physiopathology
  • Long QT Syndrome* / therapy
  • Mutation
  • NAV1.5 Voltage-Gated Sodium Channel
  • Potassium Channels / genetics
  • Potassium Channels / metabolism
  • Potassium Channels, Voltage-Gated*
  • Sodium Channels / genetics
  • Sodium Channels / metabolism
  • Trans-Activators*
  • Transcriptional Regulator ERG

Substances

  • Adrenergic beta-Antagonists
  • Cation Transport Proteins
  • DNA-Binding Proteins
  • ERG protein, human
  • ERG1 Potassium Channel
  • Enzyme Inhibitors
  • Ether-A-Go-Go Potassium Channels
  • Ion Channels
  • KCNH6 protein, human
  • NAV1.5 Voltage-Gated Sodium Channel
  • Potassium Channels
  • Potassium Channels, Voltage-Gated
  • SCN5A protein, human
  • Sodium Channels
  • Trans-Activators
  • Transcriptional Regulator ERG