Referenced in: none

Automatically associated channels: Kv11.1 , Kv7.1 , Nav1.5

Title: Fever-triggered ventricular arrhythmias in Brugada syndrome and type 2 long-QT syndrome.

Authors: A S Amin, C A Klemens, A O Verkerk, P G Meregalli, A Asghari-Roodsari, J M T de Bakker, C T January, A A M Wilde, H L Tan

Journal, date & volume: Neth Heart J, 2010 Mar , 18, 165-9

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/20390067

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.).