Fever-triggered ventricular arrhythmias in Brugada syndrome and type 2 long-QT syndrome.
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.).
Amin
A S
AS
Heart Failure Research Centre, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.
Klemens
C A
CA
Verkerk
A O
AO
Meregalli
P G
PG
Asghari-Roodsari
A
A
de Bakker
J M T
JM
January
C T
CT
Wilde
A A M
AA
Tan
H L
HL
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