Discussion
In the present study, we demonstrated that the PWD as measured just
before CIED implantation was associated with the appearance of new-onset
AHRE in the first year after CIED implantation. Specifically, longer PWD
was an independent predicting factor for the appearance of new-onset
AHRE in the multivariate analysis. The cutoff value of PWD of 48 ms as
determined by the ROC curve (area under the curve: 0.90) achieved
considerably high sensitivity and specificity values of 73.8% and
77.9%.
In this study, we detected a considerable number of patients with
new-onset AHREs in the relatively early phase after CIED implantation.
In prior studies, AHRE was defined as an episode lasting at least five
to six minutes with an atrial rate of greater than 170 to 190
beats/min,1,19,20 and we employed a similar definition
in this study. By using such criteria, the overdetection of AHREs due to
various atrial noise signals could be avoided as much as possible. In
this study, AHREs were detected in 34% of patients, which was within
the reported range of incidence of such detections over a two-year
observation period (i.e., 20%–60%).21–23
Some reports exist concerning predictors of AHREs following CIED
implantation. Prior heart failure and large LAVI were reported to be
major risk factors for the appearance of new-onset AHREs in CIED
patients.2 The ASSERT study and the Canadian Trial of
Physiologic Pacing also demonstrated that sinus node dysfunction may be
correlated with an increased risk of AHRE.5,24 The
clinical association of these diseases has been recognized for a long
time, suggesting that these diseases are associated with atrial
structural and electrical remodeling.25 In this study,
although SSS was more prevalent in the AHRE group than in the non-AHRE
group, other parameters including prior heart failure and LAVI did not
show any statistical differences between the two groups, possibly
because we excluded patients with serious structural heart disease,
which might cause atrial structural remodeling as the substrate for
AHRE. Sinus node dysfunction creates an electrophysiological substrate
that facilitates AF initiation and perpetuation.25Theoretically, prolonged PWD reflects the inhomogeneous propagation of
atrial impulses and/or the prolongation of atrial conduction time, which
may participate in the construction of the arrhythmogenic substrate of
AF. Atrial conduction disturbances can also be revealed by realizing the
conduction delay during sinus rhythm, which can be observed as
prolongation of PWD and P-wave duration. Because such prolongation in
PWD was observed even just before CIED implantation, it is suspected
that atrial electrical remodeling had already progressed in at least
some patients before CIED implantation in this study. Probably, such
electrical changes might be a precursor for the appearance of new-onset
AHRE at least in patients with CIEDs.
In a recent study, a PWD value of 40 ms was considered to be prolonged
and was correlated with physiological and/or pathological
dysfunction.26 A PWD of more than 40 ms indicates the
presence of heterogeneous electrical activity in different regions of
the atrium that might cause atrial tachyarrhythmias. Yoshizawa et al.
suggested that new-onset AF could be predicted by a PWD of more than 50
ms with a sensitivity of 69.1% and specificity of
88.2%.8 Perzanowski et al. contended that a PWD value
of 80 ms or longer was an independent predictor for AF recurrence after
cardioversion.10 Similarly, in recurrent transient
ischemic attacks, high PWD values were observed, suggesting that a PWD
of greater than 40 ms may be linked to an underlying silent paroxysmal
AF as the possible cause of ischemic recurrence. Based on these reports,
the prediction of new-onset AHRE by a PWD cutoff value of 48 mm in this
study should be considered as reasonable.
In a recent review, Pérez-Riera et al. listed some possible scenarios in
which the PWD may be prolonged and concluded that PWD is an important
and easy-to-measure parameter that indicates a greater tendency of
appearance of supraventricular arrhythmias, particularly paroxysmal
AF.26 Notably, our results in the present study match
well to one of their stated possible scenarios. Of course, there should
be some difference apparent between clinical AF and device-detected
AHRE. However, because AHRE has been reported to be associated with
increased risks of stroke, systemic embolism, and worsening heart
failure, the prediction of new-onset AHRE through PWD evaluation should
be useful in managing patients with CIED.2,5,27