Discussion
Biphasic and split P-wave prolongation during sinus rhythm have been considered as an independent predictor of the development of AF and the recurrence of AF after PV isolation.1-3 The P-wave prolongation is considered mainly to be a result of an electric conduction disturbance in the inter- or intra-atrium, and the second component of the P-wave is considered to be formed by delayed activation in the LA.4 Yanagisawa et al.1reported that the disappearance of NPW after a previous PV isolation was predictor of a durable PV isolation and that the P-wave duration was shortened after the PV isolation in patients with NPW. Another report5 suggested that a prolonged conduction time from the right atrium to the CS predicted the recurrence of AF after catheter ablation. Therefore, a prolonged P-wave duration might suggest not only an inter- or intra-atrial conduction disturbance but also the presence of a conduction delay at the structures that have electrical connections to the LA, leading to the development of an atrial arrhythmogenic substrate. On the other hand, CS musculature possesses arrhythmogenicity for triggering AF as well as other thoracic vein and forms an arrhythmogenic substrate due to multiple myocardial connections to the LA for maintaining AF.6 Catheter ablation targeting a CS region is significantly associated with AF termination and a prolongation of AF cycle length.6 It has been reported that the additional ablation strategies beyond the PV isolation fail to reduce the AF recurrence rate.7
From the anatomic and electrophysiologic viewpoint, the volume of cardiomyocytes in the CS musculature is small in comparison to that of the rest of atrium, and the electrical contribution of the CS musculature excitation on body surface ECG is limited. An electrical propagation from the proximal to distal CS during sinus rhythm is masked or fused by the LA excitation. However, in patients with a persistent left superior vena cava which has a substantial volume of cardiomyocytes, that causes changes in the P wave morphology, especially in the terminal portion of the positive/negative in lead III with significant left axis deviation.8 In addition, a significant conduction disturbance between the atrium and CS unmasks the excitation of the CS and also leads to a change in the P wave morphology. In our present case, the timing of the activation at LA appendage and lateral LA was identical to that of the first component of the P-wave, and the timing of the CS excitation was identical to that of the second component of the NPW even after the PV isolation (Figure 1B). The results of the termination and suppression of AF, and the disappearance of the second component of the P-wave with the RF application in the CS, strongly suggested that the second component of the P-wave was formed by the CS musculature activation and that the CS musculature played an important role in triggering AF.
To the best of our knowledge, this is the first report showing an NPW that was formed by the activation in the CS musculature which played a principal role in triggering and maintaining AF. In patients with repetitive recurrent AF after the establishment of the PV isolation who exhibit NPW during sinus rhythm, the CS might be one of the arrhythmogenic sources of the AF.