Sudden infant death syndrome: How significant are the cardiac channelopathies?

David J. Tester, Michael John Ackerman

Research output: Contribution to journalArticle

147 Citations (Scopus)

Abstract

Having an apparently healthy, thriving infant fail to reach his/her first birthday is profoundly tragic. This tragedy is compounded when the infant's death is unexpected and unexplained, signed out as sudden infant death syndrome (SIDS). Despite impressive success and welcome reductions in these tragic deaths due in large measure to "Back-to-Sleep" campaigns, the fundamental pathogenic mechanisms precipitating such deaths remain dimly exposed. Here, we review the causal link between SIDS and mutations involving the SCN5A-encoded cardiac sodium channel, provide new findings following extensive postmortem genetic testing of long QT syndrome (LQTS)-associated potassium channel genes in a population-based cohort of SIDS, and summarize the current understanding regarding the spectrum and prevalence of cardiac channelopathies in the pathogenesis of SIDS.

Original languageEnglish (US)
Pages (from-to)388-396
Number of pages9
JournalCardiovascular Research
Volume67
Issue number3
DOIs
StatePublished - Aug 15 2005

Fingerprint

Channelopathies
Sudden Infant Death
Long QT Syndrome
Sodium Channels
Potassium Channels
Genetic Testing
Sleep
Mutation
Population
Genes

Keywords

  • Arrhythmias
  • Forensic science
  • Ion channels
  • Long QT syndrome
  • Sudden infant death syndrome

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Sudden infant death syndrome : How significant are the cardiac channelopathies? / Tester, David J.; Ackerman, Michael John.

In: Cardiovascular Research, Vol. 67, No. 3, 15.08.2005, p. 388-396.

Research output: Contribution to journalArticle

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