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Purpose: The intrinsic atrial vulnerability is proposed as one of the mechanisms of paroxysmal atrial fibrillation (PAF) in Wolff-Parkinson-White (WPW) syndrome. In this study, we examined the early changes in atrial refractoriness and intra- and inter-atrial conduction times after radiofrequency (RF) catheter ablation of accessory pathway (AP).Methods: Twenty-four consecutive patients with WPW syndrome and documented AV reciprocating tachycardia but without history of PAF (fourteen male, mean age 39 +/- 9.5 years) and 27 control subjects (six female, mean age 51.4 +/- 10.1 years) with AV nodal reentrant tachycardia (AVNRT) who underwent ablation of the slow AV nodal pathways were enrolled into the study. Regional atrial effective refractory periods (AERPs), AERP dispersion, and intra- and inter-atrial conduction times were obtained before and 30 min after ablation and were compared between two groups. In the study group, patients with and without inducible AF were also compared regarding these parameters.Results: In the study group, AERPs in higher right atrium and right posterolateral atrium were significantly increased, and AERP dispersion, intra-atrial, and inter-atrial conduction times were significantly decreased after ablation; AERP in distal coronary sinus was unchanged. In control group, no significant difference was observed in these parameters. Inducibility of AF was significantly reduced following ablation of AP in the study group (from seven to zero of 24 patients, p = 0.016). Comparison between patients with (n = 7) and without (n = 17) AF revealed that left atrium diameter was larger, AERPs in the right posterolateral atrium before and after ablation, and ERP of AP were shorter in AF group.Conclusion: In WPW syndrome patients, RF catheter ablation of AP results in an 'immediate' decrease in atrial vulnerability. Since inducibility of AF becomes more difficult in this less vulnerable atrium, the AP itself may play an important role in the development of AF. [ABSTRACT FROM AUTHOR]

Objective: To determine whether QT dispersion (QTd), a noninvasive electrocardiographic parameter of ventricular tachyarrhythmia risk assessment, is changed by implantable cardioverter-defibrillator (ICD) shocks delivered during implantation process, to analyze the duration of these changes, and to further evaluate the effect of amiodarone on these parameters.Methods: Twenty-six consecutive patients who are scheduled to undergo ICD implantation for aborted sudden cardiac death or documented symptomatic sustained ventricular tachycardia were enrolled into the study. A simultaneous 12-lead electrocardiogram (ECG) was recorded after the ICD implantation just before starting the testing shock when the patients were under general anesthesia (baseline record) and at 1st, 5th, 10th, 15th, 20th, 25th, and 30th minutes after the successful shocks. RR interval, QT interval, corrected QT interval (QTc), QTd, and corrected QTd (QTcd) were all measured and calculated on ECG.Results: At 1st minute after the successful shock, an abrupt increase (from 67.0 +/- 13.8 ms to 94.8+/-21 ms, P < 0.0001) was observed in QTcd, which was followed by a gradual return to the preshock values at 20th minute. Analysis of patients with and without long-term oral amiodarone treatment showed that in amiodarone-pretreated patients QTcd returned to the baseline value earlier than in patients without amiodarone treatment (15 minutes vs 20 minutes, respectively).Conclusions: ICD shocks cause an increase in QTcd lasting for up to 20th minute, which may predominate in some important clinical problems like electrical storm. Amiodarone, with the desirable effect on QTcd, may reduce the proarrhythmic effects of ICD shocks. [ABSTRACT FROM AUTHOR]