IJCS | Volume 32, Nº5, September/October 2019

506 1. Dhingra RC, Amat-y-Leon F, Pietras RJ, Wyndham C, Deedwania PC, Wu D, et al. Sites of conduction disease in aortic stenosis: significance of valve gradient and calcification. Ann Intern Med. 1977;87(3):275-80. 2. Friedman HS, Zaman Q, Haft JI, Melendez S. Assessment of atrioventricular conduction in aortic valve disease. Br Heart J. 1978;40(8):911-7. References Abdelghani Conduction abnormalities afterTAVR Int J Cardiovasc Sci. 2019;32(5):505-507 Editorial paramount importance for establishing strategies to reduce the incidence of NOPCAs/NPPI after TAVR. However, this process is challenging, basically due to the diversity and the interplay of offending factors. Those factors/mechanisms can be broadly classified into patient-related, THV-related, and implantation technique-related. Patient-related factors include landing-zone anatomical features (e.g. LVOT calcium load and distribution) and anatomical and functional characteristics of the conduction system (e.g. length and course of theHis bundle andpre-existing atrioventricular or intraventricular conduction abnormalities). Device- related factors include THV platform (e.g. self- vs. balloon- vs. mechanically-expanding), device size, and extent of LVOT overstretch (a function of device oversizing). Implantation technique factors include balloon pre-dilatation and device implantation depth. Among those factors, baseline conduction defects (especially first degree heart block and right bundle branch block) and THV platform are the two most consistently identified predictors of NOPCAs/NPPI across different cohorts. 7 Beyond those causative/ predisposing factors, a major “confounding” factor contributing to NPPI rate is the clinical threshold of the operator. Operators with low thresholds to implant a permanent pacemaker (e.g. those adopting preemptive pacemaker implantation to facilitate early discharge in patients with transient atrioventricular block, new onset LBBB, or tachy-brady syndrome) usually have a considerably higher NPPI rate than their conservative peers, while adherence to guidelines on cardiac pacing leads to reduced NPPI rate after TAVR. 8 Back to the real “causative/predisposing” factors, as clinicians, we should always focus more on the modifiable factors. Amongst these, a deeper device implant is an established risk factor for the development of NOPCAs and need for NPPI. Although not addressed by Santos et al., 6 deeper (more ventricular) implantation has been shown to increase the rate of NOPCAs and NPPI with most THV platforms. While previous studies have suggested cut-points for desirable implantation depth, the concept of absolute cut-points may be overly simplified. A more logical concept would rather entail an individualized “optimal” implantation depth, which considers the anatomical vulnerability of the conduction system to mechanical injury during procedural steps. For example, in patients with left-sided atrioventricular bundle and/or short membranous septum (denoting a short distance between the aortic annulus and the bundle of His and its left branch), a shallower implant is required to avoid NOPCAs, while those with no such vulnerability may tolerate a relatively deeper implant. Beyond optimizing implantation depth, avoidance of unnecessary negative chronotropic agents periprocedurally, omitting unnecessary balloon pre-dilatation, and refraining from excessive THV oversizing (leading to overstretch of the LVOT) are further “pacemaker-sparing” strategies. The administration of anti-inflammatory/anti-edematous agents to prevent/relieve edema, hematoma, and ischemic damage of the conductive system is an appealing approach, though supportive evidence is scarce. 9-11 As mentioned earlier, watchful waiting for 3–7 days before deciding upon the need for permanent pacemaker with strict adherence to pacing guidelines can effectively reduce the number of NPPIs. TAVR has been a story of success, backed with enthusiastic motivation of clinicians to improve techniques and of manufacturers to improve technologies in order to address the limitations of TAVR. The progress in dealing with the problem of NOPCAs/ NPPI has lagged behind those achievements, largely due to protracted uncertainty regarding its prognostic relevance. Today, as the interventional community is – after all – aware of the magnitude and importance of this problem, effective handling of this shortcoming is awaited. This will require motivation of the operators to adopt “pacemaker-sparing” practices and of the manufacturers to develop technologies that address this remaining limitation of contemporary TAVR.