TY - JOUR
T1 - Electrocardiographic evidence of ventricular repolarization remodelling during atrial fibrillation
AU - Tan, Hanno L.
AU - Smits, Jeroen P. P.
AU - Loef, Arjan
AU - Tanck, Michael W. T.
AU - Hardziyenka, Maxim
AU - Campian, Maria E.
PY - 2008
Y1 - 2008
N2 - Aims Some atria[ 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 'ventricutar 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 SRbaseine. Although of limited magnitude on average (similar to 5%), the increase was substantial (similar to 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
AB - Aims Some atria[ 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 'ventricutar 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 SRbaseine. Although of limited magnitude on average (similar to 5%), the increase was substantial (similar to 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
U2 - https://doi.org/10.1093/europace/eum270
DO - https://doi.org/10.1093/europace/eum270
M3 - Article
C2 - 18094018
SN - 1099-5129
VL - 10
SP - 99
EP - 104
JO - Europace : European pacing, arrhythmias, and cardiac electrophysiology
JF - Europace : European pacing, arrhythmias, and cardiac electrophysiology
IS - 1
ER -