suad114.pdf pacing conduction system pacing

Conduction system pacing: overview, definitions,
and nomenclature
Marek Jastrzebski 1
*, Gopi Dandamudi2
, Haran Burri3
,
and Kenneth A. Ellenbogen4
1
First Department of Cardiology, Interventional Electrocardiology and Hypertension, Jagiellonian University, Medical
College, Jakubowskiego 2, 30-688 Krakow, Poland; 2
Center for Cardiovascular Health, Virginia Mason Franciscan Heath,
Seattle, WA, USA; 3
Cardiac Pacing Unit, University Hospital of Geneva, Geneva, Switzerland; and 4
Virginia
Commonwealth University Medical Center, Richmond, VA, USA
KEYWORDS
Conduction system pacing;
His bundle pacing;
Left bundle branch area
pacing;
Right bundle branch pacing;
Fascicular pacing;
Left ventricular septal
pacing
Pacing from the right ventricle is associated with an increased risk of development of
congestive heart failure, increases in total and cardiac mortality, and a worsened
quality of life. Conduction system pacing has become increasingly realized as an
alternative to right ventricular apical pacing. Conduction system pacing from the His
bundle and left bundle branch area has been shown to provide physiologic activation
of the ventricle and may be an alternative to coronary sinus pacing. Conduction
system pacing has been studied as an alternative for both bradycardia pacing and for
heart failure pacing. In this review, we summarize the clinical results of conduction
system pacing under a variety of different clinical settings. The anatomic targets of
conduction system pacing are illustrated, and electrocardiographic correlates of
pacing from different sites in the conduction system are defined. Ultimately, clinical
trials comparing conduction system pacing with standard right ventricular apical
pacing and cardiac resynchronization therapy pacing will help define its benefit and
risks compared with existing techniques.
*Corresponding author. Tel: +48 502 545 228, Email: mcjastrz@cyf-kr.
edu.pl
© The Author(s) 2023. Published by Oxford University Press on behalf of the European Society of Cardiology.
This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial License (https://
creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium,
provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com
Introduction
Chronic ventricular pacing modalities continue to evolve
in clinical practice. Although initially designed as a
life-saving measure, new indications for ventricular
pacing have been studied to try to improve morbidity and
mortality over time. However, the detrimental effects of
chronic right ventricular pacing (RVP) have also been
realized through large, randomized studies.1,2
Patients
with frequent RVP are at a significant risk of developing
pacing-induced cardiomyopathy and subsequent heart
failure (HF) symptoms.3,4
Other right ventricular (RV)
pacing locations such as the septum and outflow tract
have been studied to try to mitigate these unintended
consequences, but results have been equivocal at best.5
Biventricular pacing (BiVP) through the coronary sinus
has shown significant benefits in carefully selected
populations with left bundle branch block (LBBB) and HF
symptoms with improvement in both morbidity
and mortality.6,7
However, BiVP in other clinical cohorts
has not shown the same degree of benefit.8,9
Despite
development in lead technologies and delivery
mechanisms, approximately one-third of the patients fail
to derive clinical benefit from BiVP.
Conduction system pacing (CSP) has recently become a
popular modality to try to obviate the detrimental
effects of RVP and overcome some of the shortcomings
of BiVP (inability to place a coronary sinus lead,
diaphragmatic stimulation, suboptimal target veins,
incomplete resynchronization, etc.). Conduction system
pacing can be achieved at all levels of the conduction
system axis. His bundle pacing (HBP) has been described
as a possible pacing modality to correct underlying LBBB
in the 1970s.10,11
However, it was not until 20 years later
European Heart Journal Supplements (2023) 25 (Supplement G), G4–G14
The Heart of the Matter
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that the first clinical study was published showing the
feasibility in clinical practice.12
Patients with HF and
permanent AF with reduced left ventricular (LV) systolic
function underwent successful atrio-ventricular (AV)
nodal ablation and HBP
. Over the next decade, several
centres around the world published their data showing
the safety, feasibility, and benefits of HBP.13–17
His bundle
pacing also presents some unique challenges. The His
bundle (HB) is encased in fibrous skeleton, and specific
leads and tools are often required to pace this region.
Pacing at the atrioventricular annulus/basal septum can
result in sensing issues (poor R waves, atrial over-sensing)
and increases in pacing thresholds over time.18
Pacing of the LV septum via a trans-septal route as an
alternative pacing site for more physiological ventricular
activation was first described in 200219
and further
explored by investigators in the Netherlands.20–22
Pacing
of the proximal left bundle branch (LBB) using the
ventricular trans-septal route was first described in 2017
to overcome some of these challenges.23
Left bundle
branch area pacing (LBBAP) has been gaining significant
popularity across the world.24,25
Pacing deep within the
interventricular septum can directly engage the left
conduction system and result in normal LV activation
times, thereby preserving LV synchrony. Several large
single-centre and multi-centre observational studies
showed favourable procedural and clinical outcomes of
LBBAP both in bradycardia and HF indications.26–28
Patient cohorts that can derive particular
benefit with conduction system pacing
Frequent right ventricular pacing
As described earlier, frequent RVP (>20%) has been shown
to cause pacing-induced cardiomyopathy and increased
HF hospitalizations.3,4
In one study, there was close to a
50% reduction in HF hospitalizations in patients who
underwent HBP compared with RVP.3
In another study,
LBBAP demonstrated a hazard ratio of 0.32 in significantly
reducing the composite endpoint of HF or all-cause
mortality compared with RVP.29
Conduction system pacing
seems ideally suited to reduce the risk of pacing-induced
cardiomyopathy and subsequent HF compared with
traditional RVP. It should be noted that there are limited
data showing that BiVP is superior to RVP in patients with
preserved LV systolic function.30
Other RV pacing
locations such as the septum and outflow tract have
shown equivocal results at best.8,9
His bundle pacing was
also shown to improve the quality of life, and patients
preferred this pacing modality compared with no pacing
in a randomized trial consisting of patients with PR
intervals >200 ms, QRS ≤ 140 ms, or right bundle branch
block (RBBB) and reduced ejection fraction (EF).31
Ablate and pace strategies
Patients with symptomatic long-standing persistent atrial
fibrillation and poorly controlled heart rates can benefit
from an ‘ablate and pace’ strategy with RVP
, which
improves symptoms but does not have any effect on
EF.32,33
This strategy has been shown to reduce HF.34
In this
cohort, CSP can preserve intrinsic ventricular activation
and preserve intra-ventricular synchrony, thereby reducing
the risk of pacing-induced cardiomyopathy. Cardiac
resynchronization therapy (CRT) has been shown to have a
role in patients with permanent AF and HF with adequate
pharmacologic rate control. In the ALTERNATIVE-AF
randomized cross-over study,35
HBP was associated with
greater improvement in LV EF compared with BiVP in
patients with reduced LV EF (≤40%) and adequate rate
control.
Patients with left bundle branch block, failed
cardiac resynchronization therapy, or
non-responders
Two small, randomized trials have compared HBP with BiVP
in patients with HF and reduced EF. The His-SYNC trial was
a small pilot study that did not show any statistical
difference between the two groups in terms of
electrocardiographic or echocardiographic parameters.36
On-treatment analysis demonstrated superior electrical
resynchronization and a trend towards higher
echocardiographic response in the HBP group.37
In the
His-Alternative trial, HBP provided similar clinical and
physical improvement compared with BiVP.38
However,
pacing thresholds were higher in this group.
In a large multi-centre observational study that included
patients with EF <35%, the primary outcome (composite
endpoint of time to death or HF hospitalization) was
significantly reduced with LBBAP compared with BiVP
(20.8 vs. 28.0%).39
Also, a recent meta-analysis of all
studies comparing CSP vs. BiVP demonstrated a
significant reduction in all-cause mortality and HF
hospitalizations compared with CSP.40
Finally, CSP may be a good alternative to BiVP in patients
where traditional CRT is either not feasible or results in a
suboptimal response. Both HBP and LBBAP have shown
significant improvement with electrical resynchronization,
NYHA class, and LV EF.41
Based on the current data as outlined above, the 2021
ESC pacing guidelines42
and the 2023 HRS/APHRS/
LAHRS (Heart Rhythm Society/Asia Pacific Heart Rhythm
Society/Latin American Heart Rhythm Society)
guidelines43
on cardiac physiologic pacing for the
avoidance and mitigation of HF have endorsed CSP with
either 2a or 2b recommendations in various pacing
categories. Other populations that could potentially
benefit from CSP include patients with HF and RBBB,
patients with AV nodal disease (first-degree heart block)
with HF symptoms, and patients with intra-ventricular
conduction delay (IVCD). The clinical response rates to
either CSP or BiVP may be suboptimal in patients with
IVCD. Combining CSP with BiVP could potentially offer
better ventricular resynchronization as both the
conduction system and the myocardium are activated.44
An international collaborative study demonstrated that
this approach is safe and feasible and provides greater
electrical resynchronization compared with BiVP alone.45
Randomized trials will be needed in this particular cohort
to show long-term clinical benefits.
Anatomy of the conduction system and its
relevance to conduction system pacing
It is important to understand the anatomy of
atrioventricular conduction system to guide implantation
as well as appreciate the types of capture which may be
Overview of conducton sytem pacing G5
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obtained with CSP. Implantation technique is covered in
detail elsewhere in a recent European Heart Rhythm
Association (EHRA) consensus document,46
as well as in
another article of this supplemental issue.47
His bundle and right bundle branch
The compact atrioventricular node (AVN) lies in the
triangle of Koch, which is delimited anteriorly by the
septal tricuspid leaflet, posteriorly by the tendon of
Todaro, and at its base by the coronary sinus ostium
(Figure 1). The membranous septum forms the apex of
the triangle. The floor of the triangle of Koch is made up
by atrial myocardium, separated from the underlying
crest of the muscular inter-ventricular septum by
fibro-adipose tissue occupying the inferior pyramidal
space (which represents the ingress of epicardial tissues
from the inferior atrioventricular groove).
In an elegant autopsy study of 41 patients, Cabrera et al.49
describedvariableanatomyoftheatrioventricularconduction
axis. In a quarter of the patients, the compact AVN lay
inferiorly within the triangle of Koch. In the remaining
patients, it lay at the apex of the triangle in the
atrioventricular portion of the membranous septum. When
taking the site of penetration into the insulating tissues of
the central fibrous body as representing the transition from
the compact node to the bundle of His, the authors also
found variations in anatomy. The site of penetration was
found within the triangle of Koch in 54% of patients, whereas
penetration was at the commissure of the septal and
anterior leaflets of the tricuspid valve in 32% of patients. In
the remaining 15% of patients, the site of penetration was
within the ventricular membranous septum. In the same
report, the authors studied 60 patients to delineate the
tricuspid valve by contrast injection, while measuring the
amplitude of the His signal. The greatest amplitude was
found on the atrial aspect of the tricuspid valve in about half
of the patients and at the level of the valve insertion or in
the ventricle in the other half.49
The His bundle may
therefore be paced from the atrial aspect of the tricuspid
valve in many patients. This explains why atrial tissue may
be captured by the His lead.50
As the tricuspid valve is
inserted more apically than the mitral valve, the triangle of
Koch is a structure, which overlies the muscular crest of the
inter-ventricular septum. A lead screwed in this region may
therefore be in contact with atrial myocardium, the His
bundle, as well as ventricular myocardium and capture
these three tissues (Figure 2). Non-selective HBP (i.e. with
ventricular myocardial capture) with leads positioned in the
atrium has been demonstrated by computed tomography
(CT) scans.51
A lead, which is placed in a region with atrial
myocardium, may be prone to P-wave oversensing,52,53
which may lead to inhibition of pacing and asystole in a
pacemaker-dependent patient.
The bundle of His is ∼1.8 cm long in an adult heart and is
primarily located deep within the insulating tissue of the
central fibrous body.49,54
The central fibrous body adjoins
the membranous septum and is a continuity between the
aortic and mitral valves that extend rightwards to link
with the septal tricuspid leaflet hinge line. The tendon of
Todaro inserts into it at the apex of the Koch triangle
(Figure 1). The His bundle emerges from the central
fibrous body at the interventricular septal crest, most
often on the left side,55
and then immediately branches
into the left and right bundles in most normal hearts.
Therefore, in the majority of cases, it is the penetrating
bundle of His which is being paced. This explains why it is
important to feel torque build-up when screwing the
lead, for it to be properly fixated in the central fibrous body.
In the report by Cabrera et al.49
the membranous septum
is located between the right atrium and the LVand lacks an
inter-ventricular component in 59% of the hearts. In these
cases, there is a rapid take-off of the fascicles of the LBB at
the level of the hinge of the septal leaflet of the tricuspid
valve. In a minority of hearts, the His bundle has a
non-branching portion as it emerges from the central
fibrous body and runs a variable course on the ventricular
septum before dividing into LBB and right bundle branch
(RBB). Kawashima and Sasaki56
performed autopsies in
105 elderly patients and found 3 distinct courses of the
His bundle with respect to the membranous septum. In
47% of cases, the His bundle runs just below the inferior
border of the membranous septum under a thin layer of
myocardium; in 32%, it runs at a distance below the
membranous septum within the myocardium; and in 21%,
it is ‘naked’ and runs just below the endocardium (but is
surrounded by a fibrous sheath). This last instance
explains why His capture may be selective, even on the
ventricular aspect of the tricuspid valve.51
In the
IMAGE-HBP study,51
it was shown that almost 80% of HBP
leads were positioned on the ventricular aspect of the
tricuspid valve, on average at 5–10 mm from the tricuspid
valve plane. These findings seem at odds with the
anatomical description of the length and course of the
His bundle by Cabrera et al.,49
and it is possible that
some of these patients were in fact being paced in the
proximal RBB or that the non-branching component of
the HB is more often identified in clinical practice than in
the referenced anatomical study.
The commissure between the anterior and septal leaflets
of the tricuspid valve is adjacent to the membranous
septum,57
at proximity to the His bundle. In a case series
of five patients with HBP leads located in the ventricle,
three-dimensional echocardiography revealed that the
Figure 1 Dissection of the conduction system visualized from the
right-sided chambers. The triangle of Koch is depicted by the red dotted
triangle. Reproduced, with permission, from Cabrera et al.48
AV,
atrioventricular; CSO, coronary sinus ostium; OF, fossa ovalis; RVA, right
ventricular apex; RVOT, right ventricular outflow tract; STV, septal
leaflet of the tricuspid valve.
G6 M. Jastrzebski et al.
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leads crossed the tricuspid valve in this commissure,
without any impingement on the leaflets,58
explaining
why HBP does not increase tricuspid regurgitation.
Although the His bundle is very close to the aortic root,
being located just below the non-coronary and right
coronary cusps, there have not been any cases reported
of damage to the aortic root by HBP.
The RBB is a thin cord-like structure, which most often
splits off from the His bundle at an angle from the left
aspect of the muscular inter-ventricular septal crest and
takes a short intramuscular course within the septum
before it emerges in the sub-endocardium of the RV,
where it continues superficially in the sub-endocardium
of the septomarginal trabeculation.59
In 5/32 hearts,
Massing and James55
found that the His bundle courses
on the right side of the crest of the inter-ventricular
septum. In these cases, the RBB formed a direct
continuity with the His bundle. Pacing of the proximal
RBB has recently been described60,61
and was found in
19% of cases where HBP was originally intended.61
Left bundle branch and fascicles
The LBB immediately takes a sub-endocardial course on
the left septum, most often immediately after the His
bundle has reached the crest of the muscular ventricular
septum.48
In contrast to the RBB, the LBB has a very
variable anatomy. It usually fans out into three main
fascicles (the anterior, septal, and inferior/posterior
fascicles). The anterior fascicle is the thinnest and the
inferior fascicle the thickest (and therefore the easiest
to target for LBBAP). Unlike HBP, where the target zone
for effective pacing is very small, that of LBBAP is wide.
Based upon results of the MELOS (Multicentre European
Left Bundle Branch Area Pacing Outcomes Study)
registry,26
only 9% of patients were actually paced at the
level of the LBB. Almost 70% of patients were paced at
the fascicular level, usually at the septal and inferior
fascicles. The septum is usually thinner and easier to
penetrate at this level than more proximally. The
fascicles are surrounded by a fibrous insulating sheath
and require the lead to be in close proximity to achieve
conduction system capture. Indeed, it has been shown
by the IMAGE-LBBP study that the lead tip is most often
sub-endocardial and on average only 2 mm from the LV
blood pool.62
However, fascicular potentials were
sometimes recorded on the leads even at distances
>4 mm from the blood pool, which raises the question of
whether there are conduction system fibres which
penetrate the inter-ventricular septum. Even though this
has never been demonstrated, it is acknowledged that
terminal fibres may be under-recognized by histological
analysis owing to its destructive nature and by micro-CT
due to loss of fibrous sheaths.60
Figure 2 Illustration of His, ventricular, and atrial tissue capture by the His bundle lead. Intrinsic rhythm: sinus rhythm with preserved atrioventricular
conduction and left bundle branch block. During the threshold test with decrementing pacing output (V), various transitions were noted. NSHBP,
non-selective His bundle pacing with capture of the His bundle + local myocardium; SHBP, selective His bundle pacing with correction of left bundle
branch block and QRS displaying a right bundle branch block pattern (due to selective capture of conduction fibres destined for the left ventricle. Atrial:
lowering of pacing output resulted in capture of the right atrium only, with 1:1 atrioventricular conduction.
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The landing zone of the LBBAP lead may be on the
right-sided septum at proximity to the RBB, resulting in
transient or permanent RBB block46
Pacing lead damage
to septal perforators of the coronary arteries and veins
has been reported, with acute myocardial ischaemia
(possibly due to spasm), septal haematoma, as well as
coronary fistulas.26,46
Overview conduction system pacing capture
The conduction system of the heart can be captured
selectively (s-), i.e. without direct activation of the
adjacent myocardium or non-selectively (ns-) when local
myocardium is depolarized simultaneously with the
His-Purkinje fibres. Selective capture is diagnosed when
after the pacing spike there is an isoelectric interval
before QRS in all 12 electrocardiogram (ECG) leads. This
latency period corresponds with conduction within
His-Purkinje fibres and might be very short with distal
CSP and more prolonged with proximal CSP or in cases
with diseased, slowly conducting His-Purkinje fibres.
Lack of direct depolarization of the local myocardium
reflects itself in endocardial tracing as a non-captured
discrete local potential—because the local activation is
not simultaneous with the pacing stimulus.
Clinical significance of selective vs. non-selective capture
is not well delineated. Direct engagement of the
myocardium during non-selective capture represents the
non-physiological component of CSP
. In some clinical
scenarios, non-selective capture might be preferred over
selective capture (in progressive conduction system
disease, high conduction system capture threshold, or
as a form of compensation for the delay in activation
via the conduction system). Considering the selective
vs. non-selective dilemma, it should be noted that
non-selectivity is not a binary phenomenon. The degree of
non-selectivity varies substantially from barely noticeable
pseudo-delta wave to a dominant activation wavefront
resulting in QRS not much different from pure myocardial
paced QRS. This is because the degree of non-selectivity
depends on the interplay of two latency periods: the
latency in His-Purkinje fibres and the latency in the
adjacent working myocardium, as well as its mass.
Capture can be obtained at various levels of the
conduction system axis—as illustrated by Figure 2. Each
of these sites offers some relative advantages and
disadvantages. Little is known about the differences in
long-term clinical outcomes between these pacing
modalities. The choice of one CSP type over the other
depends on the physician preference/skills, clinical
indications, and anatomical challenges. Definitions,
nomenclature, and brief overview of various CSP capture
types are provided in Figure 3.
His bundle pacing
His bundle pacing is the most physiological CSP option. His
bundle pacing is identified when the pacing lead is
positioned in the HB region either on atrial or ventricular
side, and the criteria for HBP are met. These criteria rest
on indicating that the direct activation of the HB during
pacing is present (Table 1). His bundle pacing is
characterized by narrow paced QRS, either nearly identical
as native QRS (s-HBP) or slightly broader due to initial
pseudo-delta wave (ns-HBP) but with a smooth subsequent
activation without mid-QRS slur, notch, or plateau.63
The
hallmark of HBP is physiologically paced V6 R-wave peak
time (V6RWPT)—which serves as electrocardiographic
surrogate of local activation of the lateral wall of the LV.63
In the vast majority of HBP cases, the HB potential is
recorded, and this confirms anatomical position of the
pacing lead (His-ventricular interval ≥35 ms) and can also
serve to confirm capture of the HB. If the HB is captured,
then the interval from the pacing spike to the peak of the
V6RWPT is the same (±10 ms) as the interval from HB
potential to the V6RWPT (paced V6RWPT = native V6RWPT)
because the activation pathway from HB to the lateral wall
of the LV is identical (Figure 4).64
In cases of LBBB or
prolonged His-Ventricle (HV) interval, paced V6RWPTshould
be shorter than native V6RWPT, indicating that correction
of conduction disturbances was obtained with HBP
.
Limitations of the HBP (high capture threshold,
long-term threshold rise, poor sensing) hopefully would
be addressed by better implantation tools, matured
implantation technique, proper patient selection
(suitable anatomy, narrow QRS), and by more stringent
success criteria at implant (not accepting borderline/
high acute threshold, and unstable lead position).
Right bundle branch pacing
Right bundle branch pacing (RBBP) is defined as a direct
capture of the right-sided conduction system distal to
Figure 3 Outline of capture types obtainable at various levels of the
conduction system. HBP, His bundle pacing; LBBAP, left bundle branch
area pacing; LBPP, left bundle branch pacing; LFP, left fascicular pacing;
LVSP, left ventricular septal pacing; RBBP, right bundle branch
pacing; LAFP, left anterior fascicle pacing; LPFP, left posterior fascicle
pacing; LSFP, left septal fascicle pacing. Modified with permission from
Burri et al.46
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the HB. Right bundle branch pacing is characterized by a
short potential to ventricular electrogram interval
(usually in the range 20–34 ms), pacing lead in the
sub-endocardial area on the right side of the
inter-ventricular septum and fulfilled criteria for
conduction system capture (Table 1).61
Proximal RBBP
can be obtained inadvertently when HB is targeted and
can easily be mistaken as HBP, although these two types
of right-sided CSP can be differentiated (Table 1). Right
bundle branch pacing paced QRS is nearly always
non-selective, broader with more prominent
pseudo-delta wave. Paced RBBP V6RWPT is also longer—
reflecting slight delay in LV activation in comparison with
HBP. When the pacing site is close to the HB bifurcation,
both types of capture (HBP and RBBP) can be seen at
different outputs resulting in a double transition
pattern. Capture of very distal RBB is unlikely to have
any clinical benefit, judging by its minor effect on the
surface ECG and might easily be mistaken with RV septal
pacing.60
The diagnostic hallmark of RBBP is a mismatch
between the paced and native V6RWPT (stimulus to
V6RWPT is ≥10 ms longer than the potential to V6RWPT).
Although RBBP is less physiological than other CSP
options, it can potentially address some of the
drawbacks of HBP and left bundle branch pacing (LBBP)
and might be preferable in selected patients. Right
bundle branch pacing does not require invasive
ventricular trans-septal access to the conduction system
(in contrast to LBBP), while ample myocardium around
the RBB ensures good sensing and ‘backup’ myocardial
capture (Figure 5).
Left bundle branch pacing
Left bundle branch pacing is defined as a capture of the
pre-divisional LBB with simultaneous activation of all of
its fascicles. Since the main LBB is a sizable structure,
LBB potential should be present at the capture site, with
potential to QRS interval in the range of 25–34 ms.
Diagnosis of LBBP rests on the anatomical position of the
pacing lead and the criteria for left conduction system
Table 1 Criteria for conduction system capture
Criterion Comments SN (%) SP (%)
HBP
Absence of notch/slur/plateau in any of the
leads: I, V4–V6
Does not exclude capture with underlying non-corrected
LBBB/IVCD
67–83 92.5–96.3
Paced V6RWPT <105 ms Paced V6RWPT measured from the pacing stimulus 64.9–70.4 ∼100
ΔV6RWPT < 12 ms
(paced V6RWPT–native V6RWPT)
Native V6RWPT measured from HB potential. Not applicable
in LBBB
100 99.1
QRS transition during threshold test Non-invasive diagnostic gold standard 95 100
QRS transition during programmed stimulation
or burst pacing
Alternative method to threshold test to obtain QRS
transition
100 100
RBBP
QRS transition and any of the below:
ΔV6RWPT > 10 ms
(paced V6RWPT–native V6RWPT)
Onset of ventricular activation is due to retrograde
conduction to the HB/LBB
87.2 95.3
Double transition in QRS morphology during
threshold test
Excluding double transition due to BBB correction — —
Selective paced QRS morphology ≠ intrinsic
QRS morphology
Selective paced QRS indicative of some delay in LV
activation
— —
Potential–QRS onset interval <35 ms The shorter the interval, the higher the specificity — —
LBBP/LFP
ΔV6RWPT ≤ 10 ms Paced V6RWPT–native V6RWPT 88.2 95.4
Paced V6RWPT ≤75 ms 53 ∼100
Paced V6RWPT ≤83 ms 84.7 96.3
QRS transition during threshold test 26.4–75.4 100
QRS transition during programmed stimulation 62.1 100
QRS transition during lead deployment — —
V6–V1 ≥ 44 ms 39 ∼100
LVSP
Terminal r/R wave in V1 ∼90 —
Lead tip in the left sub-endocardial area Lead depth >1 cm within septum probably can be used as
less specific surrogate
— —
ΔV6RWPT ≥ 10 ms
(paced V6RWPT–LBBP V6RWPT)
Applicable when LBBP paced V6RWPTcan serve as reference >90 >90
LBBAP
Any of the above LVSP or LBBP/LFP criteria ∼90 —
HBP, His bundle pacing; LBBP, left bundle branch pacing; LBBAP left bundle branch area pacing; LFP, left fascicular pacing; LBBB, left bundle branch
block; V6RWPT, V6 R-wave peak time; RBBP, right bundle branch pacing; —, no data.
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capture (Table 1). Left bundle branch pacing paced QRS is
characterized by fast activation of the LV reflected by
physiological values of V6RWPT.65
Since LBBP at the
working pacing output is obligatory non-selective and
the potential to QRS period is relatively long, the direct
depolarization of the basal septal myocardium is
substantial. Left bundle branch pacing should be
differentiated from distal HBP with RBB block. This can
be accomplished based on anatomical position of the
pacing lead if distal HB is marked or by documenting
transitional paced QRS complex morphologies during
progression through the septum (phenomenon absent
during HBP). In some cases, this differentiation is
challenging and might be impossible when the lead is
placed at the HB bifurcation. Left bundle branch pacing
advantages over HBP include lower pacing thresholds,
better ventricular sensing, and the ability to reliably
recruit more patients with conduction system disease.
Left fascicular pacing
Left fascicular pacing (LFP) is defined as pacing of the left
Purkinje network created by the inter-connected fascicles
of the main LBB (Figure 6).26
Left fascicular pacing is
characterized by short potential to QRS interval (1–
25 ms) or absence of Purkinje potential. The terminal
Purkinje fibres generate small potential that might not
be recordable from the distance that the virtual pacing
electrode allows. During LFP, criteria for left conduction
system capture must be fulfilled (Table 1)—these are
based on QRS transition during dynamic manoeuvres and
on paced QRS metrics as for LBBP. Paced QRS has
minimal or no noticeable pseudo-delta wave and often
superior QRS axis. Transition to left ventricular septal
pacing (LVSP) is usually subtle as the Purkinje to
myocardium junction is close, facilitating fast
retrograde invasion. Left fascicular pacing is obtained
when the pacing lead is on the left side of the
interventricular septum, usually more mid-septal and
inferior than during LBBP. Although in cases of early
branching or ribbon fan-like LBB, capture of one of the
fascicles rather than the main LBB can be obtained
already at quite proximal/basal sites. Left fascicular
pacing area seems to offer several advantages as the
pacing lead is far away from the tricuspid valve, the
fibrous sub-annular region where lead helix
entanglement can be a problem, and larger coronary
Figure 4 V6 R-wave peak time reflects activation time of the lateral wall of the left ventricle. It remains constant during native conduction and both selective
and non-selective His bundle pacing. Loss of His bundle capture, that is right ventricular septal-only capture, results in prolongation of paced V6 R-wave peak
time by 38 ms (from 90 to 128 ms). Reproduced with permission from Jastrzebski et al.64
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arteries. Moreover, LFP area is broader and more easily
accessed and targeted than the proximal LBBP site.
MELOS found LFP the most commonly obtained site of
LBBAP capture type in real-world clinical practice.
Left ventricular septal pacing and left bundle
branch area pacing
Left ventricular septal pacing (LVSP) is defined as a capture
of the septal myocardium close to the left sub-endocardial
area, albeit without direct activation of the left
conduction system. During LVSP
, the left conduction system
is probably promptly activated (with variable delay of 5–
35 ms) via retrograde invasion. Acute LVSP studies suggest
very favourable LV activation and function despite lack of
direct activation of the conduction system.20,66
However,
lack of prompt conduction system engagement might
result in delayed activation of the lateral wall of the LV and
suboptimal outcomes, especially in patients with HF67
—this
needs to be further addressed in clinical trials. It is likely
that LVSP shows greater heterogeneity than other CSP
pacing options. Depending on where the septum is
penetrated, the obtained QRS and LV activation might vary
substantially. Left ventricular septal pacing is usually a
diagnosis of exclusion—made when there is terminal r/R
wave in lead V1 but the criteria for left CSP are not
fulfilled.46
However, diagnosis of LVSP based on these
criteria is neither 100% sensitive nor 100% specific. This is
because it is possible to obtain LVSP/LBBAP without
terminal r/R wave in lead V1,68
while in other cases, r/R in
V1 might appear already at deep septal pacing lead
positions.69
or even when pace mapping the right septal
surface.60
Therefore, diagnosis of LVSP based on the above
does not fully exclude possibility of deep septal pacing or
conduction system capture. Only in cases when LBBP/LFP
capture was obtained but was subsequently lost, the
diagnosis of LVSP can be made with high certainty because
the LBBP/LFP paced QRS can be then used as the
diagnostic reference. Left ventricular septal pacing paced
QRS compared with LFP/LBBP is characterized by several
features reflecting some deviation from physiology: usually
more prominent pseudo-delta wave and/or broader QRS,
evident repolarization abnormalities in leads I and V5–V6,
and V6RWPT longer by 10–25 ms. The term LBBAP is used to
address the common clinical scenario when differentiation
among LVSP, LBBP, and LFP is uncertain or was not properly
performed.
His bundle optimized/left bundle branch
optimized-cardiac resynchronization therapy
His bundle optimized-CRT and left bundle branch
optimized-CRT are denominations used to describe
hybrid pacing options: sequential pacing of LV
myocardium with cardiac vein lead and CSP using HBP or
LBBAP, respectively.67,70,71
These pacing modalities are used when HBP or LBBAP
alone does not result in adequate normalization of the
LV activation. This might be reflected by broad paced
Figure 5 QRS and V6 R-wave peak time difference between different His bundle area capture types. Patient with right bundle branch pacing, right bundle
branch to ventricle interval of 30 ms, and potential to V6 R-wave peak time of 82 ms. Two QRS transitions with small (<20 ms) increments of V6 R-wave peak
time were present. At high output, His bundle pacing was obtained with paced V6 R-wave peak time of 90 ms, similar to native potential to V6 R-wave peak time
of 82 ms (±10 ms). At working output, right bundle branch pacing was observed, resulting in V6 R-wave peak time increase by 10 ms. At low output, loss of right
bundle branch capture was observed resulting in right ventricular septal pacing and further increase of V6 R-wave peak time by 16 ms. Reproduced with
permission from Jastrzebski et al.61
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QRS, V6RWPT over the physiological values (>90 ms for
LBBAP and >110 ms for HBP), paced QRS notch/slur, or
lack favourable acute haemodynamic response to HBP/
LBBAP pacing alone.
Conclusions
This review focuses on clinical aspects of the anatomy
and electrocardiography of CSP
. There are several
Figure 6 Examples of paced electrocardiogram patterns and endocardial electrograms during left bundle branch area pacing. Left bundle branch pacing
characterized by left bundle branch potential to QRS interval of 34–25 ms and lead tip position ∼1.5 cm from the His bundle. Left fascicular pacing—
characterized by potential to QRS of 0–24 ms and lead tip position ∼1.5–4.5 cm from His bundle. Left bundle fascicular pacing includes: left posterior
fascicle pacing, left anterior fascicle pacing, left septal fascicle pacing. Left ventricular septal pacing: diagnosed when left bundle branch capture
criteria are not met, any distance from His bundle. Heart drawing based on work by Patrick J. Lynch and C. Carl Jaffe, MD/CC-BY 2.5, https://commons.
m.wikimedia.org/wiki/File:Heart_anterior_view_coronal_section.jpg, reproduced with permission from Jastrzebski et al.26
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randomized trials underway that will help us better
understand the benefits of CSP over both RVP and BiVP in
patients with high right ventricular apex pacing burden,
conductions system disease, and cardiomyopathy. The
electrocardiography of pacing the conduction system and
the ventricular myocardium alone and together typically
require measurements of peak R wave but also transitions
during pacing to really confirm the conduction system
capture. The highly variable anatomy of the conduction
system explains the complexity of the ECG patterns seen
with CSP.
Funding
This manuscript was published as part of a supplement
sponsored by Medtronic. The content was developed
independent of the sponsor. Authors did not receive an
honorarium.
Conflict of interest: M.J.: Honoraria, consultant –
Medtronic, Abbott, Biotronik; G.D.: Honoraria,
consultant, advisory board – Medtronic, Advisory board –
Biotronik, Abbott; H.B.: has received speaker honoraria,
consulting fees, or institutional fellowship/research
support from Abbot, BIOTRONIK, Boston Scientific,
Medtronic, and MicroPort. K.A.E.: Consultant –
Medtronic, Boston Scientific, Abbott, Biotronik;
Honoraria – Medtronic, 66 Boston Scientific, Biotronik.
Data availability
The data underlying this article will be shared on
reasonable request to the corresponding author.
References
1. Sweeney MO, Hellkamp AS, Ellenbogen KA, Greenspon AJ, Freedman
RA, Lee KL et al. Adverse effect of ventricular pacing on heart
failure and atrial fibrillation among patients with normal baseline
QRS duration in a clinical trial of pacemaker therapy for sinus node
dysfunction. Circulation 2003;107:2932–2937.
2. Wilkoff BL, Cook JR, Epstein AE, Greene HL, Hallstrom AP, Hsia H et al.
Dual-chamber pacing or ventricular backup pacing in patients with an
implantable defibrillator: the dual chamber and VVI implantable
defibrillator (DAVID) trial. JAMA 2002;288:3115–3123.
3. Abdelrahman M, Subzposh FA, Beer D, Durr B, Naperkowski A, Sun H
et al. Clinical outcomes of His bundle pacing compared to right
ventricular pacing. J Am Coll Cardiol 2018;71:2319–2330.
4. Kiehl EL, Makki T, Matar RM, Johnston DR, Rickard JW, Tarakji KG et al.
Incidence and predictors of late atrioventricular conduction recovery
among patients requiring permanent pacemaker for complete heart
block after cardiac surgery. Heart Rhythm 2017;14:1786–1792.
5. Kaye GC, Linker NJ, Marwick TH, Pollock L, Graham L, Pouliot E et al.
Effect of right ventricular pacing lead site on left ventricular function
in patients with high-grade atrioventricular block: results of the
protect-pace study. Eur Heart J 2015;36:856–862.
6. Bristow MR, Saxon LA, Boehmer J, Krueger S, Kass DA, De MT et al.
Cardiac-resynchronization therapy with or without an implantable
defibrillator in advanced chronic heart failure. N Engl J Med 2004;
350:2140–2150.
7. Cleland JG, Daubert JC, Erdmann E, Freemantle N, Gras D, Kappenberger
L et al. The effect of cardiac resynchronization on morbidity and
mortality in heart failure. N Engl J Med 2005;352:1539–1549.
8. Curtis AB, Adamson PB, Chung E, Sutton MS, Tang F, Worley S.
Biventricular versus right ventricular pacing in patients with AV
block (BLOCK HF): clinical study design and rationale. J Cardiovasc
Electrophysiol 2007;18:965–971.
9. Blanc JJ; Biopace trial investigators. Biventricular pacing for
atrio-ventricular block to prevent cardiac desynchronization. Results
Presented at European Society of Cardiology Congress, Barcelona,
Spain, September 2014.
10. El-Sherif N, Amay YL, Schonfield C, Scherlag BJ, Rosen K, Lazzara R
et al. Normalization of bundle branch block patterns by distal His
bundle pacing. Clinical and experimental evidence of longitudinal
dissociation in the pathologic his bundle. Circulation 1978;57:473–483.
11. Narula OS. Longitudinal dissociation in the His bundle. Bundle branch
block due to asynchronous conduction within the His bundle in man.
Circulation 1977;56:996–1006.
12. Deshmukh P, Casavant DA, Romanyshyn M, Anderson K. Permanent,
direct His-bundle pacing: a novel approach to cardiac pacing in patients
with normal His-Purkinje activation. Circulation 2000;101:869–877.
13. Barba-Pichardo R, Morina-Vazquez P, Fernandez-Gomez JM, Venegas-
Gamero J, Herrera-Carranza M. Permanent His-bundle pacing: seeking
physiological ventricular pacing. Europace 2010;12:527–533.
14. Kronborg MB, Mortensen PT, Gerdes JC, Jensen HK, Nielsen JC. His and
para-His pacing in AV block: feasibility and electrocardiographic
findings. J Interv Card Electrophysiol 2011;31:255–262.
15. Lustgarten DL, Calame S, Crespo EM, Calame J, Lobel R, Spector PS.
Electrical resynchronization induced by direct His-bundle pacing.
Heart Rhythm 2010;7:15–21.
16. Sharma PS, Dandamudi G, Naperkowski A, Oren JW, Storm RH,
Ellenbogen KA et al. Permanent His-bundle pacing is feasible, safe,
and superior to right ventricular pacing in routine clinical practice.
Heart Rhythm 2015;12:305–312.
17. Keene D, Arnold AD, Jastrzebski M, Burri H, Zweibel S, Crespo E et al.
His bundle pacing, learning curve, procedure characteristics, safety,
and feasibility: insights from a large international observational
study. J Cardiovasc Electrophysiol 2019;30:1984–1993.
18. de Leon J, Seow SC, Boey E, Soh R, Tan E, Gan HH et al. Adopting
permanent His bundle pacing: learning curves and medium-term
outcomes. Europace 2022;24:606–613.
19. Grosfeld MJ, Res JC, Vos DH, de Boer TJ, Bos HJ. Testing a new
mechanism for left interventricular septal pacing: the transseptal
route; a feasibility and safety study. Europace 2002;4:439–444.
20. Mafi-Rad M, Luermans JG, Blaauw Y, Janssen M, Crijns HJ, Prinzen FW
et al. Feasibility and acute hemodynamic effect of left ventricular
septal pacing by transvenous approach through the interventricular
septum. Circ Arrhythm Electrophysiol 2016;9:e003344.
21. Mills RW, Cornelussen RN, Mulligan LJ, Strik M, Rademakers LM,
Skadsberg ND et al. Left ventricular septal and left ventricular
apical pacing chronically maintain cardiac contractile coordination,
pump function and efficiency. Circ Arrhythm Electrophysiol 2009;2:
571–579.
22. Peschar M, de Swart H, Michels KJ, Reneman RS, Prinzen FW. Left
ventricular septal and apex pacing for optimal pump function in
canine hearts. J Am Coll Cardiol 2003;41:1218–1226.
23. Huang W, Su L, Wu S, Xu L, Xiao F, Zhou X et al. A novel pacing
strategy with low and stable output: pacing the left bundle branch
immediately beyond the conduction block. Can J Cardiol 2017;33:
1736.e1.
24. Kircanski B, Boveda S, Prinzen F, Sorgente A, Anic A, Conte G et al.
Conduction system pacing in everyday clinical practice: EHRA
physician survey. Europace 2023;25:682–687.
25. Keene D, Anselme F, Burri H, Perez OC, Curila K, Derndorfer M et al.
Conduction system pacing, a European survey: insights from clinical
practice. Europace 2023;25:euad019.
26. Jastrzebski M, Kielbasa G, Cano O, Curila K, Heckman L, De PJ et al.
Left bundle branch area pacing outcomes: the multicentre European
MELOS study. Eur Heart J 2022;43:4161–4173.
27. Padala SK, Master VM, Terricabras M, Chiocchini A, Garg A, Kron J et al.
Initial experience, safety, and feasibility of left bundle branch area
pacing: a multicenter prospective study. JACC Clin Electrophysiol
2020;6:1773–1782.
28. Su L, Wang S, Wu S, Xu L, Huang Z, Chen X et al. Long-term safety and
feasibility of left bundle branch pacing in a large single-center study.
Circ Arrhythm Electrophysiol 2021;14:e009261.
29. Sharma PS, Patel NR, Ravi V, Zalavadia DV, Dommaraju S, Garg V et al.
Clinical outcomes of left bundle branch area pacing compared to right
ventricular pacing: results from the Geisinger-Rush Conduction System
Pacing Registry. Heart Rhythm 2021;19:3–11.
30. Yu CM, Chan JY, Zhang Q, Omar R, Yip GW, Hussin A et al. Biventricular
pacing in patients with bradycardia and normal ejection fraction. N
Engl J Med 2009;361:2123–2134.
Downloaded
from
by
guest
on
05
April
2024

31. Whinnett ZI, Shun-Shin MJ, Tanner M, Foley P, Chandrasekaran B,
Moore P et al. Effects of haemodynamically atrio-ventricular
optimized His bundle pacing on heart failure symptoms and exercise
capacity: the His optimized pacing evaluated for heart failure
(HOPE-HF) randomized, double-blind, cross-over trial. Eur J Heart
Fail 2023;25:274–283.
32. Huang W, Wang S, Su L, Fu G, Su Y, Chen K et al. His-bundle pacing vs
biventricular pacing following atrioventricular nodal ablation in
patients with atrial fibrillation and reduced ejection fraction: a
multicenter, randomized, crossover study—the ALTERNATIVE-AF trial.
Heart Rhythm 2022;19:1948–1955.
33. Weerasooriya R, Davis M, Powell A, Szili-Torok T, Shah C, Whalley D et al.
The Australian intervention randomized control of rate in atrial
fibrillation trial (AIRCRAFT). J Am Coll Cardiol 2003;41:1697–1702.
34. Kay GN, Ellenbogen KA, Giudici M, Redfield MM, Jenkins LS, Mianulli M
et al. The Ablate and Pace Trial: a prospective study of catheter
ablation of the AV conduction system and permanent pacemaker
implantation for treatment of atrial fibrillation. APT investigators. J
Interv Card Electrophysiol 1998;2:121–135.
35. Brignole M, Menozzi C, Gianfranchi L, Musso G, Mureddu R, Bottoni N
et al. Assessment of atrioventricular junction ablation and VVIR
pacemaker versus pharmacological treatment in patients with heart
failure and chronic atrial fibrillation: a randomized, controlled
study. Circulation 1998;98:953–960.
36. Upadhyay GA, Vijayaraman P, Nayak HM, Verma N, Dandamudi G, Sharma
PS et al. His corrective pacing or biventricular pacing for cardiac
resynchronization in heart failure. J Am Coll Cardiol 2019;74:157–159.
37. Upadhyay GA, Vijayaraman P, Nayak HM, Verma N, Dandamudi G,
Sharma PS et al. On-treatment comparison between corrective His
bundle pacing and biventricular pacing for cardiac resynchronization:
a secondary analysis of the His-SYNC Pilot Trial. Heart Rhythm 2019;
16:1797–1807.
38. Vinther M, Risum N, Svendsen JH, Mogelvang R, Philbert BT. A
randomized trial of His pacing versus biventricular pacing in
symptomatic HF patients with left bundle branch block
(His-alternative). JACC Clin Electrophysiol 2021;7:1422–1432.
39. Vijayaraman P, Sharma PS, Cano O, Ponnusamy SS, Herweg B, Zanon F
et al. Comparison of left bundle branch area pacing and biventricular
pacing in candidates for resynchronization therapy. J Am Coll Cardiol
2023;82:228–241.
40. Kim JA, Kim SE, Ellenbogen KA, Vijayaraman P, Chelu MG. Clinical
outcomes of conduction system pacing versus biventricular pacing
for cardiac resynchronization therapy: a systematic review and
meta-analysis. J Cardiovasc Electrophysiol 2023;34:1718–1729.
41. Sharma PS, Dandamudi G, Herweg B, Wilson D, Singh R, Naperkowski A
et al. Permanent His-bundle pacing as an alternative to biventricular
pacing for cardiac resynchronization therapy: a multicenter
experience. Heart Rhythm 2018;15:413–420.
42. Glikson M, Nielsen JC, Kronborg MB, Michowitz Y, Auricchio A, Barbash
IM et al. 2021 ESC guidelines on cardiac pacing and cardiac
resynchronization therapy. Europace 2022;24:71–164.
43. Chung MK, Patton KK, Lau CP, Dal Forno ARJ, Al-Khatib SM, Arora V,
et al. 2023 HRS/APHRS/LAHRS guideline on cardiac physiologic
pacing for the avoidance and mitigation of heart failure. Heart
Rhythm 2023;20:e17–e91.
44. Zweerink A, Zubarev S, Bakelants E, Potyagaylo D, Stettler C,
Chmelevsky M et al. His-optimized cardiac resynchronization therapy
with ventricular fusion pacing for electrical resynchronization in heart
failure. JACC Clin Electrophysiol 2021;7:881–892.
45. Vijayaraman P, Herweg B, Verma A, Sharma PS, Batul SA, Ponnusamy
SS et al. Rescue left bundle branch area pacing in coronary venous
lead failure or nonresponse to biventricular pacing: results from
international LBBAP collaborative study group. Heart Rhythm 2022;
19:1272–1280.
46. Burri H, Jastrzebski M, Cano O, Curila K, De PJ, Huang W et al. EHRA
clinical consensus statement on conduction system pacing
implantation: endorsed by the Asia Pacific Heart Rhythm Society
(APHRS), Canadian Heart Rhythm Society (CHRS), and Latin American
Heart Rhythm Society (LAHRS). Europace 2023;25:1208–1236.
47. Huang W, Keene D, Vijayaraman P. Implant, assessment and
management of conduction system pacing. Eur Heart J 2023.
48. Cabrera JA, Anderson RH, Porta-Sanchez A, Macias Y, Cano O, Spicer
DE et al. The atrioventricular conduction axis and its implications
for permanent pacing. Arrhythm Electrophysiol Rev 2021;10:181–189.
49. Cabrera JA, Anderson RH, Macias Y, Nevado-Medina J, Porta-Sanchez A,
Rubio JM et al. Variable arrangement of the atrioventricular conduction
axis within the triangle of Koch: implications for permanent His bundle
pacing. JACC Clin Electrophysiol 2020;6:362–377.
50. Burri H, Jastrzebski M, Vijayaraman P. Electrocardiographic analysis
for His bundle pacing at implantation and follow-up. JACC Clin
51. Vijayaraman P, Dandamudi G, Subzposh FA, Shepard RK, Kalahasty G,
Padala SK et al. Imaging-based localization of his bundle pacing
electrodes: results from the prospective IMAGE-HBP study. JACC Clin
52. Bakelants E, Burri H. Troubleshooting programming of conduction
system pacing. Arrhythm Electrophysiol Rev 2021;10:85–90.
53. Burri H, Keene D, Whinnett Z, Zanon F, Vijayaraman P. Device
programming for His bundle pacing. Circ Arrhythm Electrophysiol
2019;12:e006816.
54. Scherlag BJ, Lazzara R. Functional aspects of His bundle physiology
and pathophysiology: clinical implications. J Electrocardiol 2017;50:
151–155.
55. Massing GK, James TN. Anatomical configuration of the His bundle and
bundle branches in the human heart. Circulation 1976;53:609–621.
56. Kawashima T, Sasaki H. A macroscopic anatomical investigation of
atrioventricular bundle locational variation relative to the
membranous part of the ventricular septum in elderly human hearts.
Surg Radiol Anat 2007;27:206–213.
57. Mulpuru SK, Cha YM, Asirvatham SJ. Synchronous ventricular pacing
with direct capture of the atrioventricular conduction system:
functional anatomy, terminology, and challenges. Heart Rhythm
2016;13:2237–2246.
58. Hasumi E, Fujiu K, Kawata T, Komuro I. The influence of His bundle
pacing on tricuspid valve functioning using three-dimensional
echocardiography. HeartRhythm Case Rep 2018;4:437–438.
59. Nagarajan VD, Ho SY, Ernst S. Anatomical considerations for His bundle
pacing. Circ Arrhythm Electrophysiol 2019;12:e006897.
60. Burri H, Kozhuharov N, Jastrzebski M. Proximal and distal right bundle
branch pacing: insights into conduction system physiology.
HeartRhythm Case Rep 2023;9:372–375.
61. Jastrzebski M, Kielbasa G, Moskal P, Bednarek A, Rajzer M, Curila K
et al. Right bundle branch pacing: criteria, characteristics, and
outcomes. Heart Rhythm 2023;20:492–500.
62. Chen K, Liu X, Hou X, Qiu Y, Lin J, Dai Y et al. Computed tomography
imaging-identified location and electrocardiographic characteristics
of left bundle branch area pacing in bradycardia patients. J
Cardiovasc Electrophysiol 2022;33:1244–1254.
63. Jastrzebski M, Moskal P, Curila K, Fijorek K, Kukla P, Bednarek A et al.
Electrocardiographic characterization of non-selective His-bundle
pacing: validation of novel diagnostic criteria. Europace 2019;21:
1857–1864.
64. Jastrzebski M, Moskal P, Kukla P, Bednarek A, Kielbasa G, Rajzer M
et al. Novel approach to diagnosis of His bundle capture using
individualized left ventricular lateral wall activation time as
reference. J Cardiovasc Electrophysiol 2021;32:3010–3018.
65. Jastrzebski M, Kielbasa G, Curila K, Moskal P, Bednarek A, Rajzer M
et al. Physiology-based electrocardiographic criteria for left bundle
branch capture. Heart Rhythm 2021;18:935–943.
66. Salden FCWM, Luermans JGLM, Westra SW, Weijs B, Engels EB,
Heckman LIB et al. Short-term hemodynamic and
electrophysiological effects of cardiac resynchronization by left
ventricular septal pacing. J Am Coll Cardiol 2020;75:347–359.
67. Jastrzebski M, Moskal P, Huybrechts W, Curila K, Sreekumar P,
Rademakers LM et al. Left bundle branch-optimized cardiac
resynchronization therapy (LOT-CRT): results from an international
LBBAP collaborative study group. Heart Rhythm 2022;19:13–21.
68. Vijayaraman P, Ponnusamy SS. Masked right bundle branch conduction
delay pattern during left bundle branch pacing. Heart Rhythm 2022;
19:2027–2029.
69. Curila K, Burri H. Left ventricular septal pacing—can we trust the ECG?
Indian Pacing Electrophysiol J 2023;23:155–157.
70. Vijayaraman P, Herweg B, Ellenbogen KA, Gajek J. His-optimized cardiac
resynchronization therapy to maximize electrical resynchronization: a
feasibility study. Circ Arrhythm Electrophysiol 2019;12:e006934.
71. Zweerink A, Burri H. His-optimized and left bundle branch-optimized
cardiac resynchronization therapy: in control of fusion pacing. Card
Electrophysiol Clin 2022;14:311–321.
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on
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