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Inherited cardiac arrhythmia syndromes: what have they taught us about arrhythmias and anti-arrhythmic therapy?

Abstract
1. In recent years, the identification of the gene defects in a vast array of monogenic disorders has revolutionized our understanding of the basic mechanisms underlying numerous disease processes. 2. Mutations in cardiac ion channels have been identified as the basis of a wide range of inherited arrhythmia syndromes, including the congenital long QT syndromes, Brugada syndrome, Lenegre syndrome, Andersen's disease and familial atrial fibrillation. 3. Identification of mutations in the human-ether-a-go-go-related gene (HERG) K(+) channel as the molecular basis of congenital long QT syndrome type 2 also led to the discovery that HERG is the molecular target for the vast majority of drugs (both cardiac and non-cardiac) that cause drug-induced arrhythmias. This has had profound implications not only for the development of anti-arrhythmic agents, but also for drug development in general. 4. The sequencing of the human genome in a sense represents the pinnacle of the reductionist era of molecular medicine. The great challenge now is to re-integrate the information gathered during the 'reductionist era' to provide a better understanding of the intact organism. Computer modelling is likely to be a key component of that re-integration process.
AuthorsRajesh N Subbiah, Terence J Campbell, Jamie I Vandenberg
JournalClinical and experimental pharmacology & physiology (Clin Exp Pharmacol Physiol) Vol. 31 Issue 12 Pg. 906-12 (Dec 2004) ISSN: 0305-1870 [Print] Australia
PMID15659058 (Publication Type: Congress)
Chemical References
  • Anti-Arrhythmia Agents
Topics
  • Animals
  • Anti-Arrhythmia Agents (therapeutic use)
  • Arrhythmias, Cardiac (drug therapy, genetics, physiopathology)
  • Humans
  • Syndrome

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