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