Key result
Complete radiofrequency ablation of the AV node significantly prolonged the mean QT interval at 30 minutes postablation compared to 1 month (482 vs 446 ms, P<0.05), unlike in bradycardia controls.
Why the study?
Does AV node ablation cause time-dependent prolongation of ventricular repolarization in patients with rapid atrial arrhythmias?
Cohort (n=20)
Does AV node ablation cause time-dependent prolongation of ventricular repolarization in patients with rapid atrial arrhythmias?
p-value: p=<0.05
AV node ablation causes a transient, relative increase in ventricular repolarization duration that stabilizes after 24 hours, suggesting a potential mechanism for postprocedural sudden death.
Transient QT prolongation after AV node ablation may warrant 24-hour monitoring; leaves open its contribution to postprocedural sudden death.
Although effective, there is a disturbing incidence of sudden death after AV node ablation. The mechanism may be related to proarrhythmia associated with prolongation in ventricular repolarization from the sudden decrease in heart rate. To examine this issue, we studied 15 patients undergoing complete radiofrequency ablation of the AV node for rapid atrial arrhythmias. Twelve-lead ECGs of paced rhythms at rates of 60, 80, 100, and 120 beats/min were recorded at time points of 30 minutes, 24 hours, 1 week, and 1 month after ablation. The QT interval was measured in the limb and precordial leads with the best T wave offset. The change in the QT interval (delta QT) relative to the measurement at 30-minute postablation was calculated. For comparison, a similar procedure was performed on patients receiving pacemakers for primary bradycardia (n = 5). The mean QT interval at 60 beats/min, 30-minutes postablation was significantly longer than at time points thereafter (482 +/- 39 vs 446 +/- 28 ms at 1 month, limb leads, for example, P < 0.05). Analysis of delta QT revealed a significant shortening of the QT interval at nearly every paced rate at every time point relative to the value at 30-minute postablation. The QT intervals shortened and stabilized after 24 hours. Neither the QT interval nor delta QT changed significantly in patients paced for primary bradycardia. We conclude that there is a relative increase in the duration of ventricular repolarization after AV node ablation, which then decreases and stabilizes after 24 hours. Such changes are not seen in patients being paced for primary bradycardia. This data is consistent with the hypothesis that sudden death after AV node ablation may be related to proarrhythmia from prolonged ventricular repolarization.
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Dizon et al. (2000) conducted a cohort in Rapid atrial arrhythmias (n=20). Complete radiofrequency ablation of the AV node vs. Patients receiving pacemakers for primary bradycardia was evaluated on Mean QT interval at 60 beats/min (p=<0.05). Complete radiofrequency ablation of the AV node significantly prolonged the mean QT interval at 30 minutes postablation compared to 1 month (482 vs 446 ms, P<0.05), unlike in bradycardia controls.
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