Tan Hanno L, Smits Jeroen P P, Loef Arjan, Tanck Michael W T, Hardziyenka Maxim, Campian Maria E
Department of Clinical and Experimental Cardiology, Heart Failure Research Center, Academic Medical Center, University of Amsterdam, Meibergdreef 9, 1105 AZ Amsterdam, The Netherlands.
Europace. 2008 Jan;10(1):99-104. doi: 10.1093/europace/eum270. Epub 2007 Dec 19.
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.
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 (SR(baseline)), immediately after termination of AF (SR(postAF)), and at follow-up (SR(followup): > or =7 days after SR(postAF)). Moreover, we studied determinants of QTc prolongation at SR(postAF). We found that, in all groups, QTc at SR(postAF) was significantly and transiently prolonged compared with SR(baseline). Although of limited magnitude on average (approximately 5%), the increase was substantial (approximately 15%) in some individuals. The only independent predictor of the magnitude of QTc prolongation was QTc duration at SR(baseline); this relation had a negative correlation.
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.
一些心房颤动（AF）患者在房颤终止后立即服用延长QTc的抗心律失常药物（IA/III类）时，会出现QTc过度延长和尖端扭转型室速。我们推测这是由房颤期间心室复极的变化引起的。我们旨在确定是否发生了这种“心室复极重塑”。
我们研究了在30个月期间因房颤就诊于我们心脏急诊室并转为窦性心律（SR）的所有患者。我们定义了四组：（i）未使用抗心律失常药物，电复律（n = 30），（ii）未使用抗心律失常药物，房颤自发终止（n = 19），（iii）使用抗心律失常药物，电复律（n = 29），以及（iv）使用抗心律失常药物，房颤自发终止（n = 9）。我们研究了房颤前SR时的QTc间期（SR（基线））、房颤终止后立即的QTc间期（SR（房颤后））以及随访时的QTc间期（SR（随访）：SR（房颤后）后≥7天）。此外，我们研究了SR（房颤后）时QTc延长的决定因素。我们发现，在所有组中，与SR（基线）相比，SR（房颤后）时的QTc均显著且短暂延长。尽管平均幅度有限（约5%），但在一些个体中增加幅度较大（约15%）。QTc延长幅度的唯一独立预测因素是SR（基线）时的QTc间期；这种关系呈负相关。
房颤导致心室复极重塑，导致QTc延长。QTc延长在一些患者中很显著，可能使这些患者在房颤终止后立即容易受到IA/III类抗心律失常药物致心律失常作用的影响。
