His bundle pacing in humans was first described in 1970 by
Narula et al. They demonstrated that it was possible to stimulate the His
bundle to produce normal physiological ventricular activation via the
His-Purkinje system. However, the first report of permanent His bundle pacing,
by Deshmukh et al., did not occur until 2000. In that study, His pacing was
performed in a series of patients with impaired left ventricular systolic
function and AF prior to atrioventricular (AV) node ablation.
The lack of dedicated tools for implantation initially
hampered enthusiasm; however, the development of specially designed sheaths and
leads for delivering permanent His bundle pacing has led to a renewed interest.
The potential role of His pacing in heart failure is large: it may prevent the
development of pacing-induced cardiomyopathy; it may be used as an alternative
to biventricular pacing in patients with heart failure and left bundle branch
block (LBBB); and it may extend pacing therapy in heart failure to patients with
narrow QRS and PR prolongation by providing AV synchrony without inducing
ventricular dyssynchrony.
His Bundle Pacing: Conduction System and Outcomes (A)
Schematic representation of the His-Purkinje conduction system. The membranous
septum is indicated in yellow. Image courtesy of K. Shivkumar, MD, PhD, UCLA
Cardiac Arrhythmia Center, Wallace A. McAlpine MD collection. Reproduced with
permission. (B) Clinical outcomes of HBP. Kaplan-Meyer survival curves
demonstrating a statistically significant reduction in the primary endpoint
(composite endpoint of all-cause mortality, HFH, or upgrade to biventricular
pacing) with His bundle pacing (HBP) compared with right ventricular pacing
(RVP) in all patients and in patients with ventricular pacing (VP) >20%.
Reprinted from Abdelrahman et al. (62). AVN = atrioventricular node; CS =
coronary sinus; HB = His bundle; IVC = inferior vena cava; LBB = left bundle
branch; LV = left ventricle; PA = pulmonary artery; RA = right atrium; RBB =
right bundle branch; SVC = superior vena cava
Anatomy of the His Bundle and Implant Technique
The bundle of His extends from the compact AV node to the
membranous interventricular septum, and measures approximately 20 mm in length.
The bundle is a cord-like structure made up of multiple strands, which, even
before the branching, are predestined to become the right or left bundle
branches. His bundle pacing can be achieved by placing the lead at the atrial
portion against the septum.
The most commonly used lead for His bundle pacing is the 69
cm Select Secure™ 3830 (Medtronic). This is a non-stylet-driven active fixation
lead. Importantly, the screw forms part of the tip electrode allowing
penetration of the capsule of the bundle of His and, therefore, direct
stimulation of the His bundle fibres. The lead can be delivered to the His
bundle region using either the specially-designed non-deflectable His delivery
sheath (C315 43 cm; Medtronic) or a deflectable sheath (C304 69 cm; Medtronic).
Unlike traditional lead placement that primarily uses fluoroscopic guidance,
His lead placement primarily uses electrical mapping. An electrogram from the
lead tip is displayed using placement via either a lab electrophysiology system
or a standard pacing system analyser.
A His signal is targeted, aiming for the local ventricular
electrogram to be approximately twice the amplitude of the atrial signal . To
confirm successful His capture, a 12-lead ECG is used to assess the QRS
morphology with pacing. Criteria used to establish whether His capture has
occurred are well described.Recently-published data suggests thresholds of
<2.5 at 1 ms should be achieved. An increase in pacing threshold is observed
in ~10 % of patients, leading to shorter battery duration. There is also a
higher rate of lead revisions (6.7 %) due to loss of capture or increased
threshold.
Anatomic Variations of the His Bundle
Despite recent advances and interest in HBP, several
unanswered questions and concerns remain . Although permanent HBP may be an
attractive option for physiological pacing in several groups of patients, its
reliability and long-term performance are yet to be fully validated in large
prospective studies. Particularly relevant are patients with infranodal,
intra-Hisian AV block and BBB, where long-term safety of HBP has not been well
studied. In such patients, should a backup RV lead be placed with HBP? What
happens to the His bundle when it is traumatized by the screw on the tip of the
lead in the long term? Can a second His Bundle pacing lead be placed
successfully if the earlier lead fails in the long run? Considerable effort
needs to go into improving the design and structure of the lead and the
delivery tools to allow for easier implantation and stabilization of the lead.
Beyond implant, what are the implications of extracting a chronic HBP lead? And
beyond pacing hemodynamics, what is the impact of HBP on arrhythmia? Does HBP
reduce the risk of ventricular tachyarrhythmias in the presence of myocardial
scar? These and other questions remain.
What is certain is that this technique holds potential and
requires further validation in larger studies with longer follow-up. It is also
clear that collective and collaborative efforts from physician scientists,
industry partners, scientific societies, and regulatory authorities will be
required to successfully develop this technology and advance our understanding
of the physiology of pacing.
Conclusions
HBP is an attractive mode of physiological pacing with
significant promise for future applications in patients who are traditional
candidates for RV pacing as well as CRT. Widespread adaptation of this
technique is dependent on the improvement of tools and further validation of
its efficacy in large randomized clinical trials.
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