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Europace Advance Access originally published online on December 19, 2007
Europace 2008 10(1):99-104; doi:10.1093/europace/eum270
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2007. For permissions please email: journals.permissions@oxfordjournals.org

ELECTROCARDIOGRAPHY

Electrocardiographic evidence of ventricular repolarization remodelling during atrial fibrillation

Hanno L. Tan1,2,*, Jeroen P.P. Smits2, Arjan Loef3, Michael W.T. Tanck4, Maxim Hardziyenka1 and Maria E. Campian1

1 Department of Clinical and Experimental Cardiology, Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands; 2 Department of Cardiology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; 3 Department of Hospital Pharmacy, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands; 4 Department of Clinical Epidemiology, Biostatistics and Bioinformatics, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands

Aims: Some atrial fibrillation (AF) patients develop excessive QTc prolongation and torsade de pointes when they take QTc-prolonging antiarrhythmic drugs (class IA/III) immediately after termination of AF. We hypothesized that this is caused by changes in ventricular repolarization during AF. We aimed to establish whether such ‘ventricular repolarization remodelling’ occurs.

Methods and results: We studied all patients who visited our cardiac emergency room with AF and converted to sinus rhythm (SR) in a 30 months’ period. We defined four groups: (i) no antiarrhythmic drugs, electrical cardioversion (n = 30), (ii) no antiarrhythmic drugs, spontaneous AF termination (n = 19), (iii) antiarrhythmic drugs, electrical cardioversion (n = 29), and (iv) antiarrhythmic drugs, spontaneous AF termination (n = 9). We studied QTc duration at SR before AF (SRbaseline), immediately after termination of AF (SRpostAF), and at follow-up (SRfollowup: ≥7 days after SRpostAF). Moreover, we studied determinants of QTc prolongation at SRpostAF. We found that, in all groups, QTc at SRpostAF was significantly and transiently prolonged compared with SRbaseline. Although of limited magnitude on average (~5%), the increase was substantial (~15%) in some individuals. The only independent predictor of the magnitude of QTc prolongation was QTc duration at SRbaseline; this relation had a negative correlation.

Conclusion: AF causes ventricular repolarization remodelling, resulting in QTc prolongation. QTc prolongation is substantial in some patients and may render these patients vulnerable to pro-arrhythmia from class IA/III antiarrhythmic drugs immediately after termination of AF.

Key Words: Atrial fibrillation, QT interval, Long QT syndrome, Remodelling

* Corresponding author. Tel: +31 20 5663264; fax: +31 20 6975458. E-mail address: h.l.tan{at}amc.nl

Manuscript submitted 31 August 2007. Accepted after revision 15 November 2007.


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