I read with great interest the recently published article by Özderya et al. titled, “A new and easy parameter to predict the requirement for permanent pacemaker implantation after transaortic valve implantation: aortic knob calcification” [1]. The authors have made a significant contribution to the literature by identifying aortic knob calcification (AKC) as a cost-effective and easily accessible predictor for the need for permanent pacemaker (PPM) implantation following transcatheter aortic valve implantation (TAVI). The findings of the study are particularly noteworthy for their potential clinical utility. This not only aligns with current trends in minimizing procedural risks but also adds a novel perspective to preoperative assessments. However, I am of the opinion that additional clarification on a number of points would further enhance the clinical applicability of the study.
Firstly, the study appears to have primarily focused on patients with tricuspid aortic valves, with only a minimal number of bicuspid aortic valve (BAV) patients included. Given the anatomical and pathological features of BAVs, such as increased calcification of raphes and asymmetric leaflet fusion, and their younger age compared with tricuspid patients [2], it is unclear whether AKC would be similarly predictive in BAV patients. Similarly, there was no statistically significant difference in the mortality rates observed in the study groups. However, it is questionable whether an 18-month follow-up period is sufficient to demonstrate this outcome with statistical significance. TAVI-related conduction disturbance requiring new PPM implantation has been associated in some studies with increased mortality and rehospitalization rates [3]. The aforementioned result regarding mortality may result in an underestimation of the unfavourable outcomes associated with long-term RV pacing in patients, particularly those with BAV. Therefore, extrapolating the study’s findings to the whole TAVI population may not be appropriate without further validation.
Additionally, non-coronary cusp (NCC) calcification, which is a well-known determinant of PPM due to its anatomical proximity to the conduction system [4], was not found to be a determinant in this study. The study does not provide information on the measurement of NCC calcification. However, in studies showing NCC as a predictor of PPM after TAVI, NCC was analysed as NCC-device landing zone calcium volume [5]. Therefore, it might be confusing that “NCC calcification”, which is an anatomical parameter due to its proximity to the conduction system, was not a predictor of PPM because of incomplete evaluation of its volume in this study, whereas AKC was a predictor of PPM.
Furthermore, there are reports in the literature indicating an association between AKC and ischaemic stroke [6]. Given that the transcatheter heart valve systems traverses the aorta, the inclusion of data on post-TAVI stroke would have considerably enhanced the value of the publication.
In conclusion, while the study by Özderya et al. represents a valuable contribution to the existing literature, addressing the aforementioned points could enhance its utility for clinicians. I believe that addressing these issues will strengthen the intended conclusions of the study and provide readers with a more comprehensive perspective on the management of the risk of post-TAVI PPM implantation.
