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Cardiovascular Research 2005 67(3):388-396; doi:10.1016/j.cardiores.2005.02.013
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Copyright © 2005, European Society of Cardiology

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

David J. Tester and Michael J. Ackerman*

Departments of Medicine, Pediatrics, and Molecular Pharmacology and Experimental Therapeutics and the Divisions of Cardiovascular Diseases and Pediatric Cardiology, Mayo Clinic College of Medicine, United States

* Corresponding author. Sudden Death Genomics Laboratory, Guggenheim 501, Mayo Clinic, Rochester, MN 55905, United States. Tel.: +1 507 284 0101; fax: +1 507 284 3757. Email address: ackerman.michael{at}mayo.edu

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.

KEYWORDS Sudden infant death syndrome; Long QT syndrome; Ion channels; Arrhythmias; Forensic science

* The National Institutes of Health (HD42569), American Heart Association (Established Investigator Award), Doris Duke Charitable Foundation, the Dr. Scholl Foundation, the CJ Foundation for SIDS and the Mayo Foundation supported Dr. Ackerman's research program.

Time for primary review 25 days


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