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.