Human congenital long QT syndrome: More than previously thought?

Bernard Attali*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review


Mutations in KCNQ1 and KCNE1, the α- and β-subunits of the IKS K+ channel, produce the cardiac long QT (LQT) syndrome. These subunits are expressed in heart and inner ear, but also in epithelial tissues such as kidney or intestine where their functional roles have remained elusive. Recent work has shown that KCNE1-deficient mice display chronic hypokalemia and hyperaldosteronism. These results have significant implications for human congenital LQT syndromes because hypokalemia increases the risk of ventricular arrhythmia and cardiac sudden death.

Original languageEnglish
Pages (from-to)249-251
Number of pages3
JournalTrends in Pharmacological Sciences
Issue number6
StatePublished - 1 Jun 2002


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