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01-03-2010 | Interuniversity Cardiology Institute of the Netherlands | Uitgave 3/2010

Netherlands Heart Journal 3/2010

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

Tijdschrift:
Netherlands Heart Journal > Uitgave 3/2010
Auteurs:
A. S. Amin, C. A. Klemens, P. G. Meregalli, A. Asghari-Roodsari, J. M. T. de Bakker, C. T. January, A. A. M. Wilde, H. L. Tan
Belangrijke opmerkingen
Heart Failure Research Centre, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, and Interuniversity Cardiology Institute Netherlands
Heart Failure Research Centre, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands
Departments of Medicine and Physiology, Cellular and Molecular Arrhythmia Research Program, University of Wisconsin, Madison, Wisconsin, USA
Heart Failure Research Centre, Department of Experimental Cardiology, and Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands

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.)

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Netherlands Heart Journal

Het Netherlands Heart Journal wordt uitgegeven in samenwerking met de Nederlandse Vereniging voor Cardiologie en de Nederlandse Hartstichting. Het tijdschrift is Engelstalig en wordt gratis beschikbaa ...

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