Discussion
This case report describes the occurrence of a perimembranous VSD associated with HBP, a complication of HBP which has not been reported previously. HBP becomes widely adopted as an alternative for RV pacing, yielding a clear physiological benefit for pacemaker therapy. Safety assessments of HBP have mainly focused on pacing thresholds, lead dislodgments and the subsequent need for lead revisions.5, 6 To the best of our knowledge, the impact of HBP leads on the integrity of the interventricular septum has not been investigated. HBP requires the lead to be screwed in at the His bundle region. The His bundle runs along the membranous interventricular septum before dividing into the bundle branches at the crest of the muscular interventricular septum.8 However, the course of the His bundle along the membranous septum varies among patients as does the amount of overlying myocardial tissue. Kawashima et al described three distinct types of HB anatomy and course in relation to the membranous septum.4 In type I and type II His bundle anatomy the His bundle is surrounded by a thin and thick layer of myocardial tissue, respectively, and runs on the inferior border of the membranous septum. In patients with a type III His bundle anatomy (25% of the cases), the His bundle runs just below the endocardial surface of the thin membranous ventricular septum and is not surrounded by myocardial fibers (“naked His bundle”). In those patients, the target zone for HBP, guided by the largest His bundle potential, will guide the implanter towards the thin membranous part of the septum. Placement of a pacing lead at this position might be more prone to lead perforation given the fragility of the membranous. Our case presented with S-HBP at both low and high output at the first HBP implant attempt. As we were not able, even at high pacing output, to capture the septal myocardium (only S-HBP was possible), this patient is suspected to have a type III His bundle anatomy. The absence of macro-dislocation on fluoroscopy and the inability to capture the His bundle on the unipolar tip configuration three weeks after implant, suggests perforation of the HBP lead through the membranous septum. As an echocardiography was not performed before the lead explantation, we cannot exclude that the VSD resulted from the HBP lead removal itself. However, the first HBP lead could be unscrewed easily 3 weeks after implant and was removed with simple traction and without any resistance. Nonetheless, the experience with removal of HBP leads is limited at this moment. Recently, Vijayaraman et al. reported a high success rate of lead extraction of 3830 leads implanted on the HBP. No procedure-related complications occurred in their series, and re-implantation of the HBP lead was successful in the majority of patients, indicating limited damage to the conduction tissue by extraction. However, it was not specified whether the ventricular septum was assessed by echocardiography for occurrence of asymptomatic VSD.
Based on the restrictive character of the VSD in this patient, surgical closure seems not indicated. However, restrictive VSDs might present a future risk for late endocarditis, aortic regurgitation or development of a double-chambered right ventricle and should therefore not be considered harmless.9 An iatrogenic (peri)membranous VSD is also less likely to close spontaneously.10 The incidence and risks of VSD associated with HBP is currently not known, but the occurrence of this complication may trigger the discussion regarding the optimal position of a pacing lead in the ventricular septum to achieve physiological pacing. A HBP lead resulting in NS-HBP, indicating capture of both His Purkinje and adjacent septal myocardial tissue, might be less prone to septal perforation as it probably suggests an implant site more distal towards the thicker muscular septum. Our patient had S-HBP at low and high pacing output, indicating that the lead was presumably screwed in at the thin membranous septum. Of interest, previous studies, comparing S-HBP and NS-HBP, did not report any advantage of S-HBP over NS-HBP in terms of ventricular synchrony or clinical endpoints.11, 12 Therefore, a better safety profile of NS-HBP with less risk for VSD together with the potential of myocardial capture in case of loss of His bundle capture, might favor HBP implants with non-selective His bundle capture responses. Recently, left bundle branch pacing (LBBP) and left ventricular septal (LVS) pacing have been proposed as an alternative pacing modality to achieve physiologic pacing.13-15With both LBBP and LVSP, the lead is screwed more distally into the muscular septum towards the left side of the septum. Compared to HBP, pacing at the left side of the ventricular septum is associated with lower pacing thresholds, better R wave sensing, absence of atrial or His bundle oversensing and lead stability.14 Although perforations have been reported when targeting a pacing lead towards the left side of the septum, they generally remain without consequences.14 Even if a muscular VSD occurs, the chance of spontaneous VSD closure is higher than with membranous VSDs10, as closure depends on muscular overgrowth.
Pacing the conduction system or the left side of the septum are novel strategies that should be monitored for rare complications such as VSD. Our case highlights the importance of routine echocardiographic screening for unintended complications that may occur in these novel pacing strategies, especially in the setting of de novo exit block or increased pacing thresholds during follow up.