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Dispersions of repolarization and ventricular arrhythmogenesis: lessons from animal models

Matthew J Killeen1, Ian N Sabir, Andrew A Grace

  • 1Cardiovascular Research Centre, Massachusetts General Hospital, 149 13th Street, Charlestown, MA 02129, USA. matthew.killeen@gmail.com

Progress in Biophysics and Molecular Biology
|November 26, 2008
PubMed

Insights

Sudden cardiac death from ventricular arrhythmias is a major concern. This review explores repolarization abnormalities in Long QT Syndrome (LQTS) and the use of mice to study these life-threatening cardiac arrhythmias.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Genetics

Background:

  • Sudden cardiac death due to ventricular arrhythmias causes significant mortality.
  • Long QT Syndrome (LQTS) involves inherited/acquired ion channel dysfunction.
  • Impaired cardiac repolarization in LQTS leads to arrhythmias.

Purpose of the Study:

  • To review the mechanisms of arrhythmias caused by repolarization heterogeneities.
  • To explore the utility of the mouse model in studying LQTS arrhythmias.

Main Methods:

  • Literature review of cardiac electrophysiology and arrhythmia mechanisms.
  • Analysis of studies utilizing genetically modified mouse models for LQTS research.

Main Results:

  • Repolarization abnormalities create a substrate for lethal arrhythmias.
  • Mouse models offer a genetically tractable platform to investigate these mechanisms.

Conclusions:

  • Understanding repolarization heterogeneities is key to preventing sudden cardiac death.
  • The mouse model is valuable for dissecting the genetic and molecular basis of LQTS-related arrhythmias.

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