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.