Sinus node dysfunction (i.e., chronotropic incompetence) is the most common indication for pacemaker implantation,1 with remarkable potential to relieve associated symptoms. Based on the DAVID II trial, we are comfortable with high atrial pacing burdens, and liberally apply rate-responsive programming to restore physiologic heart rates without concern for deleterious effects on myocardial function.2 The liberties afforded with atrial pacing do not apply in the ventricle, and prior to permanent His bundle pacing (PHBP), we lacked good options for patients requiring ventricular pacing.
RV apical pacing causes interventricular dyssynchrony and adverse hemodynamics.3 Progression to pacing-induced cardiomyopathy (PICM) over months to years may be anticipated for pacing burden >20% and paced QRS >150 msec,4,5 with increased congestive heart failure (CHF) and atrial fibrillation proportional to the pacing burden.6,7 Given the detrimental effects of RV pacing, a variety of algorithms have been developed to minimize RV pacing (Vp Suppression®, BIOTRONIK; RYTHMIQ™, Boston Scientific; SafeR™, ELA Medical/Sorin Group; Managed Ventricular Pacing (MVP®), Medtronic; and Ventricular Intrinsic Preference (VIP™), St. Jude Medical). Paradoxically, the success of the pacemaker is measured by how little pacing occurs. While these algorithms may achieve important reductions in RV pacing, the resulting loss of AV synchrony becomes another source of impaired cardiac function.
It is regrettable to implant a pacing lead in the RV apex when a substantial ventricular pacing burden is anticipated. However, better options have not been apparent, as alternate site (high septal) pacing also proved disappointing.8 Biventricular pacing may be an alternative, but implanting a CRT-P system seems excessive when ventricular function is preserved, as this represents additional hardware and battery drain due to higher thresholds characteristic of LV leads. When PICM occurs, patients are typically offered a CRT-P upgrade at the next device changeout. This may not occur for years following the onset of cardiomyopathy, resulting in substantial morbidity. While CRT-P may be compensatory,3 biventricular pacing introduces a non-physiologic ventricular activation sequence, which may also result in deterioration of ventricular function (increased left ventricular end-systolic volume index, or LVESVI) and increased presentations for CHF.9,10
PHBP is rapidly emerging as an ideal solution to the problems associated with ventricular pacing. Heart failure hospitalization is dramatically reduced (2% vs 15%) with PHBP compared to RV apical pacing, with a trend towards mortality benefit.11 PHBP directly engages the His-Purkinje system (HPS), utilizing normal physiology to maintain synchronous ventricular activation, without concern for ensuing cardiomyopathy. While PHBP has been performed almost exclusively at some centers for years,12 adoption of the technique is hardly universal. We performed PHBP for the first time in Washington State on June 9, 2016. We also performed the first known case of PHBP with Closed Loop Stimulation (CLS; BIOTRONIK) on June 23, 2016, combining what may be the most physiologic algorithm for rate-responsive pacing with the most physiologic pacing site. The implant procedure is not difficult for operators familiar with His potential recording and slittable sheaths, and outcomes are very rewarding. In this article we share our early experience, with the goal to encourage other centers to adopt PHBP.
Presently, only Medtronic offers a specialized lead and the delivery tools necessary for PHBP. The SelectSecure 3830 His lead (Medtronic) is lumenless with a 1.8-mm exposed helix, and therefore requires a delivery sheath for placement (Figure 1). The fixed-curve C315 His sheath (Medtronic) is most commonly used (Figures 1A, 1B, and 1E). The C315 has both a proximal curve toward the tricuspid valve (TV) annulus and a second curve toward the septum, so the lead can be fixed perpendicularly with excellent tissue contact. Cephalic, axillary, or subclavian venous access is possible, with a 7 French (Fr) introducer sheath. The SelectSite C304 deflectable sheath (Medtronic) serves as an alternate (Figures 1C and 1D), and is introduced with a 9 Fr sheath. The C304 is particularly useful to reach the His bundle in the setting of a dilated right atrium. Approval for MRI is anticipated, when the lead is used with an Advisa pulse generator (Medtronic).
The His sheath is advanced to the TV annulus over a guidewire, which is then replaced with the 3830 lead. With the sheath tip directed superiorly and septally, the lead tip is advanced beyond the tip of the sheath (Figure 2A). A unipolar connection (Figure 1E) is used to map and record His potentials (Figure 3) through the pace-sense analyzer (PSA), which may be identified using gentle rotation and micromanipulation of the external sheath. We used a CRD-2™ (St. Jude Medical) His catheter from the femoral vein to locate a His signal in advance and guide lead placement during our first 10 cases, and continue to do so when difficult anatomy is anticipated (Figures 2A-C). In routine cases, the contribution of the His catheter is minimal. Lower amplitude ventricular EGMs (1.2-10 mV) are acceptable, and active fixation is achieved with 4-5 clockwise rotations of the lead body, which is expected to unwind 1-2 rotations when released.12 The sheath is then pulled back without placing tension on the lead, so the lead can form a loop in the atrium (Figure 2B). Higher pacing thresholds are considered acceptable (≤2 V @ 1 ms),12 and the His sheath is removed using the slitting mechanism. With His bundle (HB) capture, HV and Stimulus to V intervals should be the same. The basal position (Figures 8A and 8D) and septal orientation (Figures 8B and 8C) of the lead tip can be appreciated relative to a conventional pacing lead. Inadvertent entrapment of the lead in the tricuspid valve prevents the lead from appropriately looping in the right atrium (Figures 2D-F). Active fixation should be reversed with lead repositioning to obtain a lead profile with adequate slack (Figure 2C).
While smaller ventricular EGMs and higher pacing thresholds would be subpar for an RV apical lead, these may represent features of a high-quality PHBP implant, given the local anatomy. The His bundle courses through the membranous septum encased in a fibrous sheath, which may be 0.5 cm above the plane of the tricuspid valve with only sleeves of myocardium extending to this site.13 Larger ventricular EGMs are recorded when the lead is slightly more apical relative to the His, which may be necessary when adequate characteristics cannot be obtained at more annular sites, resulting in pacing of septal myocardium rather than HBP. Small atrial EGMs are frequently recorded in unipolar mode, and disappear in bipolar mode. Testing should be performed in both unipolar and bipolar configurations, ensuring that atrial capture does not occur at high output.12
It is important to watch for His bundle injury current at implant. His potentials are identified prior to active fixation (Figure 3A), and may display injury current post fixation (Figure 3B). In prior series, His injury current was seen in nearly 40% of cases, and resulted in long-term pacing thresholds significantly lower than those without injury current at implant.14 We document whether His potentials were recorded and the presence of injury in each procedure report, which may aid in understanding chronic lead characteristics. We have not found pacing thresholds to be particularly elevated when His bundle injury is not observed (Figure 3C).
Greater than 80% success with HBP has been reported, with similar fluoroscopy times compared to conventional pacemaker implantation (12.7 ± 8 min vs 10 ± 14 min; P=.14), and 5% lead revision rate. Chronic pacing thresholds were higher in the HBP group than in the RVP group (1.35 ± 0.9 V vs 0.6 ± 0.5 V at 0.5 ms; P<.001) and remained stable over a two-year follow-up period.11,14 The time for HB lead implantation (16 minutes) was shorter than standard left ventricular lead implantation time (42 minutes).15 HB pacing thresholds are lower than LV thresholds with CRT, such that battery life is spared with PHBP relative to CRT.
The success of PHBP is ultimately determined by the morphology of the paced QRS complex. In the absence of bundle branch block or interventricular conduction delay, PHBP may perfectly reproduce the intrinsic QRS, or result in a morphologically similar QRS due to non-selective capture of adjacent myocardium. In the latter case, non-selective capture results in early basal-septal action, but this is superceded by early engagement of rapid HPS conduction, retaining the benefits of PHBP. Pure HB capture is frequently observed over a range of pacing outputs, which may change with lead maturation, with non-specific capture occurring at higher or lower outputs.12 With pre-existing conduction system disease, PHBP may significantly normalize the QRS, while the biventricular paced QRS remains wider and morphologically very different (mean QRS duration: native 171 ± 13 ms, DHBP 148 ± 11 ms, BiV 158 ± 21, P<.0001).15
QRS narrowing with PHBP is best explained by capture of latent His-Purkinje tissue, consistent with early demonstrations that distal His pacing may normalize left bundle branch block (LBBB) (25% of patients).16 Figure 4 shows PHBP in the setting of complete heart block. The paced QRS was identical to the intrinsic QRS at all outputs, representing an ideal outcome. Figure 5 shows PHBP with pure His capture occurring only at very low pacing outputs. Finding pure His capture at any output strongly suggests that the full benefits of PHBP will result even with non-specific capture at the programmed output. We have also observed QRS narrowing dependent on AV delay. Figure 6 shows pre-existing bundle branch block evident with prolonged AV delays, with QRS narrowing when the AV delay was shortened. AV search hysteresis was disabled to retain maximal benefit from PHBP.
PHBP may be ideal in the setting of PICM resulting from RV apical pacing, which is anticipated for RV pacing >20% and paced QRS >150 msec,4,5 with advantages over CRT upgrade (discussed above). Figure 7 shows upgrade of a single-chamber ICD to PHBP using a CRT-D device, in a patient with cardiomyopathy who developed >80% ventricular pacing dependence. A HB pacing lead was implanted and plugged into the LV port. An LV offset of -80 msec was programmed, causing the RV stimulus to fall in the refractory period, such that only PHBP occurred.12 The patient will be followed for any recovery of LV function.
Atrioventricular Junction (AVJ) Ablation
PHBP is often performed when AVJ ablation is planned. Figure 8 shows PHBP with a backup pacing lead in the RV apex, should failure of HB pacing occur. The HB lead was plugged into the atrial port and an RV apical lead was plugged into the ventricular port. Using a BIOTRONIK pacemaker, impedance measurements for the CLS rate response algorithm were obtained from the RV apex, with rate-responsive pacing delivered by the HB lead. The post-atrial blanking period (PABP) may be shortened to allow RV sensing and inhibition of pacing in the RV apex. Alternately, RV pacing during the refractory period will occur. In this setting, AVJ ablation is performed close to the site of lead fixation, where interactions may result in increased threshold or loss of capture. We have used electroanatomic mapping to ensure adequate separation and to direct ablation towards the compact AV node (Figure 9).
PHBP promises to transform pacemaker therapy, permitting high ventricular pacing burden with little concern for PICM relative to RV apical pacing. PHBP may also be used for CRT; however, routine use is limited by uncertainty in the level of block underlying an observed LBBB or RBBB pattern, and whether distal His pacing will adequately reverse the block. In cases of failed LV lead implantation, PHBP may be considered rather than referring for epicardial lead placement, with the HB lead plugged into the LV port of CRT devices. The implant procedure is not difficult for operators facile with His potential recording and slittable sheaths, with implant times approaching those of conventional pacemakers.
Acknowledgements. Thank you to Toni Evans, Kristie Larios, and Janelle Thorndike for device support, and to Ashley Weller for assisting with manuscript preparation.
Disclosures: The author has no conflicts of interest to report regarding the content herein. Outside the submitted work, Dr. Kneller reports personal fees from Medtronic and BIOTRONIK.
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- Wilkoff BL, Kudenchuk PJ, Buxton AE, et al. The DAVID (Dual Chamber and VVI Implantable Defibrillator) II Trial. J Am Coll Cardiol. 2009;53(10):872-880.
- Sohaib SMA, Wright I, Lim E, et al. Atrioventricular optimized direct his bundle pacing improves acute hemodynamic function in patients with heart failure and PR prolongation without left bundle branch block. JACCEP. 2015;1(6):582-591.
- Khurshid S, Epstein AE, Verdino RJ, et al. Incidence and predictors of right ventricular pacing-induced cardiomyopathy. Heart Rhythm. 2014;11:1619-1625.
- Khurshid S, Liang JJ, Owens A, et al. Longer Paced QRS Duration is Associated With Increased Prevalence of Right Ventricular Pacing-Induced Cardiomyopathy. J Cardiovasc Electrophysiol. 2016;27(10):1174-1179.
- Wilkoff BL, Cook JR, Epstein AE, 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(24):3115-123.
- Sweeney MO, Hellkamp AS, Ellenbogen KA, 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(23):2932-2937.
- Kaye GC, Linker NJ, Marwick TH, 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(14):856-862.
- Curtis AB, Worley SJ, Adamson PB, et al. Biventricular pacing for atrioventricular block and systolic dysfunction. N Engl J Med. 2013;368(17):1585-1593.
- Doshi RN, Daoud EG, Fellows C, et al. Left ventricular-based cardiac stimulation post AV nodal ablation evaluation (the PAVE study). J Cardiovasc Electrophysiol. 2005;16(11):1160-1165.
- Sharma PS, Dandamudi G, Naperkowki A, et al. Permanent His-bundle pacing is feasible, safe, and superior to right ventricular pacing in routine clinical practice. Heart Rhythm. 2015;12(2):305-312.
- Dandamudi G, Vijayaraman P. How to perform permanent His bundle pacing in routine clinical practice. Heart Rhythm. 2016;13:1362-1366.
- Correa de Sa DD, Hardin NJ, Crespo EM. Autopsy analysis of the implantation site of a permanent selective direct his bundle pacing lead. Circ Arrhythm Electrophysiol. 2012;5(1):244-246.
- Vijayaraman P, Dandamudi G, Worsnick S, et al. Acute His-Bundle Injury Current during Permanent His-Bundle Pacing Predicts Excellent Pacing Outcomes. Pacing Clin Electrophysiol. 2015;38(5):540-546.
- Lustgarten DL, Calame S, Crespo EM, et al. Electrical resynchronization induced by direct His-bundle pacing. Heart Rhythm. 2010;7(1):15-21.
- Narula OS. Longitudinal Dissociation in the His Bundle. Circulation. 1977;56:996-1006.