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

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

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)165-169
Number of pages5
JournalNetherlands Heart Journal
Issue number3
Publication statusPublished - Mar 2010


  • Brugada syndrome
  • Fever
  • Long QT syndrome
  • Tachycardia
  • Ventricular

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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