title: Fever-triggered ventricular arrhythmias in Brugada syndrome and type 2 long-QT syndrome.
abstract: The risk for lethal ventricular arrhythmias is increased in individuals who carry mutations in genes that encode cardiac ion channels. Loss-of-function mutations in SCN5A, the gene encoding the cardiac sodium channel, are linked to Brugada syndrome (BrS). Arrhythmias in BrS are often preceded by coved-type ST-segment elevation in the right-precordial leads V1 and V2. Loss-of-function mutations in KCNH2, the gene encoding the cardiac ion channel that is responsible for the rapidly activating delayed rectifying potassium current, are linked to long-QT syndrome type 2 (LQT-2). LQT-2 is characterised by delayed cardiac repolarisation and rate-corrected QT interval (QTc) prolongation. Here, we report that the risk for ventricular arrhythmias in BrS and LQT-2 is further increased during fever. Moreover, we demonstrate that fever may aggravate coved-type ST-segment elevation in BrS, and cause QTc lengthening in LQT-2. Finally, we describe molecular mechanisms that may underlie the proarrhythmic effects of fever in BrS and LQT-2. (Neth Heart J 2010;18:165-9.).
authors.affiliation: Heart Failure Research Centre, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
authors.forename: A S
authors.initials: AS
authors.lastname: Amin
authors.forename: C A
authors.initials: CA
authors.lastname: Klemens
authors.forename: A O
authors.initials: AO
authors.lastname: Verkerk
authors.forename: P G
authors.initials: PG
authors.lastname: Meregalli
authors.forename: A
authors.initials: A
authors.lastname: Asghari-Roodsari
authors.forename: J M T
authors.initials: JM
authors.lastname: de Bakker
authors.forename: C T
authors.initials: CT
authors.lastname: January
authors.forename: A A M
authors.initials: AA
authors.lastname: Wilde
authors.forename: H L
authors.initials: HL
authors.lastname: Tan
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