With interest, we took notice of the paper by Buellesfeld et al. (1) investigating the impact of permanent pacemaker implantation on clinical outcome after transcatheter aortic valve implantation (TAVI) (1). The authors state that periprocedural permanent pacemaker (PPM) implantation does not affect rate of death, stroke, and/or myocardial infarction at 12 months compared with patients with pre-existing PPM or patients without any PPM. Because the findings of present study seem to contrast with earlier observations from the MOST (Mode Selection Trial) study and the DAVID (Dual Chamber and VVI Implantable Defibrillator) trial, we have some concerns regarding the study design ((2),3).

First of all, Buellesfeld et al. (1) do not provide a power calculation regarding the study size. Given the relatively low number of patients, it is likely that the study is under-powered to detect differences in the primary endpoint of all-cause mortality. It is plausible than an endpoint combining all-cause mortality with hospitalization for worsening of heart failure would have resulted in different outcome between the groups. Indeed, the MOST and DAVID trials, using similar endpoints, demonstrated that chronic right ventricular pacing is associated with occurrence of heart failure ((2),3).

Second, the PPM implantation strategy in the present study seems rather liberal and early, with almost three-quarters of implantations occurring within 3 days after TAVI. As early atrioventricular conduction disorders post-TAVI are known to recover over time ((4),(5),6), a considerable number of patients would have received a PPM unnecessarily. Although scarce, there is some evidence that during longer follow-up of TAVI-related PPM implantations, patients show no or limited pacemaker dependency (7) (unpublished data van der Boon RM, van Mieghem NM, Theuns DA, et al., 2012). Due to alterations in pacing mode, these patients are not exposed to the unbeneficial effects of chronic right ventricle pacing.

We recently compared the impact of TAVI-induced left bundle branch block (LBBB) on all-cause mortality during long-term follow-up. In a cohort of 679 patients, all-cause mortality was significantly higher among patients with TAVI-induced LBBB compared with patients without LBBB. Interestingly, the mortality rate among patients receiving PPM after TAVI was comparable to that of patients without TAVI-induced LBBB. This discrepancy could be explained by the low percentage of cumulative ventricular pacing in the PPM group (8).

In conclusion, in the present study by Buellesfeld et al. (1), patient classification might be problematic as the post-TAVI PPM patients are principally heterogeneous and are not all exposed to the risks of (continuous) right ventricular pacing, which might explain the findings of the current study. We agree with the authors that larger-scaled studies are needed to further investigate the impact of PPM after TAVI.