His Bundle Pacing at Hartford Healthcare Heart and Vascular Institute

Introduction

Permanent His bundle pacing (HBP) in humans was first described by Deshmukh in 2000.¹ Despite steady expansion of the evidence base underlying the technique, clinical adoption over the last 18 years has been slow. In part, this is due to the impression that HBP is overly complex and not easy to achieve. The reality is that, while there are certainly nuances to HBP, the technique is not necessarily more complicated than any of the other advanced electrophysiologic procedures that are routinely performed every day in EP labs.  

At the Hartford Healthcare Heart and Vascular Institute, we have engaged with Medtronic to provide the His Bundle Pacing Virtual Proctorship program in order to provide a resource for physicians looking to learn the procedure. Approximately once per month, live HBP cases are broadcast from Hartford Hospital. Physicians are able to remotely “tune in” to the procedure via WebEx, and they can ask questions that are answered in real time. During these sessions, we review the tools, implant techniques, and different pacing responses seen during HBP. Over the last year, we have had nearly 200 participants from a variety of countries take part in these sessions. Edited recordings of representative teaching cases have also been made available online at Medtronic Academy; these recordings can be viewed at www.MedtronicAcademy.com/hisbundlepacing.

Below we present a case which we believe highlights the utility of HBP, and which represents a great example of why we are so enthusiastic about this form of pacing.

Case Presentation

A 76-year-old male with a severely stenotic bicuspid aortic valve, ascending aortic aneurysm, and persistent atrial fibrillation underwent a Bentall procedure with aortic root reconstruction, bioprosthetic aortic valve replacement, and a concomitant Maze procedure in March 2016. At the time he presented for his procedure, he was in atrial fibrillation with a narrow QRS of 102 ms (Figure 2). His post-operative course was complicated by persistent complete heart block, and a dual-chamber pacemaker was implanted. An echocardiogram prior to discharge demonstrated normal prosthetic valve function, mild left ventricular hypertrophy, and a normal ejection fraction (EF) of 60%. 

From a clinical standpoint, he did well for the first year, but then began to develop fatigue and exertional dyspnea. An echocardiogram performed in September 2017 (18 months post-op) demonstrated that although the prosthetic aortic valve function was normal, his left ventricle had become dilated with reduced function (EF 35%) and that moderate/severe mitral regurgitation had developed. At this point, the clinical suspicion was that he had developed a pacing-induced cardiomyopathy. Therefore, he was referred for evaluation for cardiac resynchronization therapy (CRT). His ECG at the time of CRT evaluation is shown in Figure 3. The paced QRS was quite wide at 178 ms.

The patient was brought to the EP lab in November 2017. The plan at that time of presentation was to attempt His bundle pacing, with a backup of traditional CRT if His bundle pacing should prove unobtainable. Given the lack of an escape rhythm, it was not possible to map the His location in the usual fashion. Instead, a pace mapping approach was utilized. 

Once venous access had been obtained, a C315 His sheath (Medtronic) was advanced to the AV groove via a 7 French peel-away sheath. A 3830 pacing lead (Medtronic) was then advanced to the tip of the sheath, and pace mapping was performed in a unipolar fashion (tip-to-pocket) utilizing the prosthetic aortic valve as an anatomical landmark. Using this approach, sites with non-selective His bundle capture were readily located, but most had unacceptably high capture thresholds. After trying several sites, a location with acceptable parameters was finally found.

The leads were connected to a CRT-pacemaker (Percepta CRT-P MRI, Medtronic), with the His lead placed into the LV port. The VV offset was programmed to 80 ms. This programming ensured that the RV lead would only serve as a backup since, barring loss of His lead capture, the RV lead would pace into refractory tissue.

At the end of the procedure, there was non-selective HPB with His capture down to 2.75V at 1 ms. There was continued basal RV septal capture down to 1V at 1 ms. The His pacing output was programmed to 5V at 1 ms. By the next day, the His capture threshold had improved to 2V at 1 ms with RV capture down 1V at 1 ms. The immediate post-operative ECG is shown in Figure 4, and an ECG at 3 months post-op is shown in Figure 5. Note the normalization of the T waves on the latter tracing. The location of the His pacing lead relative to the aortic valve is shown in Figure 6.

The patient began to have symptomatic improvement within weeks of upgrade, with resolution of his fatigue and exertional dyspnea. An echocardiogram done 3 months following the procedure showed normalization of LV size and function (EF 55%), with only trace mitral regurgitation. Pacing parameters at 3 months remained stable, and the His pacing output was programmed to 3V at 1 ms. 

Discussion

The detrimental effects of frequent RV pacing have long been recognized,² with the frequency of pacing-induced cardiomyopathy (PICM) estimated to approach 20%.³ The traditional approach to these patients is to add a left ventricular lead to the system in order to affect CRT. Although this approach is generally successful, LV lead placement is not always possible, and not all patients respond to CRT. An alternative approach is to “upgrade” the existing system to provide HBP.

Permanent His bundle pacing leverages the patient’s native conduction system in order to provide truly physiologic ventricular pacing.⁴ The technique for His bundle pacing has been well described.⁵ Briefly, the 3830 (69 cm) lead is directed to the His bundle region via a fixed curve C315 His (43 cm) sheath, or in more challenging anatomies, a deflectable C304 sheath (Medtronic). Unipolar mapping and pacing can then be performed (tip-to-pocket). Intracardiac electrograms are reviewed on both the pace-sense analyzer (PSA) and EP recording system. Although the use of only the PSA is feasible, an EP recording system allows for visualization of a full surface 12-lead ECG, which is extremely helpful in analyzing pacing morphologies in order to determine whether His bundle capture has been achieved.

Shan et al recently explored the feasibility and clinical outcomes of upgrading to HBP in a prospective cohort of 18 patients with PICM or CRT non-responders.⁶ Among these patients, successful His bundle pacing was achieved in 16 (88.9%). HBP resulted in a significantly narrower QRS duration, and at 1 year, the LV dimensions had decreased from baseline (LVIDd 55.5 ± 7.7 mm from 62.3 ± 6.9 mm) and ejection fraction had substantially improved (52.8% ± 9.6% from 35.7% ± 7.9%). They also reported a decrease in the severity of mitral regurgitation. There were no major complications during implantation. Given that the results of CRT upgrade among patients with PICM have been mixed,^7,8 studies such as this suggest that HBP offers a viable, and perhaps superior, alternative to CRT in this patient population. While a definitive answer to this question awaits the results of future studies, HBP should be considered when patients present with PICM.

Disclosures: Dr. Zweibel reports fees from Medtronic to the hospital for virtual preceptorship on His bundle pacing; outside the submitted work, he also discloses he is a speaker and consultant for Medtronic. Dr. Crespo reports receiving honoraria from Medtronic for educational talks on His bundle pacing.

References

1. Deshmukh P, Casavant RA, 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.
2. Sweeney MO, Hellkamp AS, Ellengogen 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;107:2932-2937.
3. Khurshid S, Epstein AE, Verdino RJ, et al. Incidence and predictors of right ventricular pacing-induce cardiomyopathy. Heart Rhythm. 2014;11:1619-1625.
4. Dandamudi G, Vijayaraman P. History of His bundle pacing. J Electrocardiol. 2017;50:156-160.
5. Lustgarten DL. Stepwise approach to permanent His bundle pacing. J Innov Card Rhythm Manage. 2016;7:2313-2321.
6. Shan P, Su L, Zhou X, et al. Beneficial effects of upgrading to His bundle pacing in chronically paced patients with left ventricular ejection fraction <50%. Heart Rhythm. 2018;15:405-412.
7. Kiehl EL, Makki T, Kumar R, et al. Incidence and predictors of right ventricular pacing-induced cardiomyopathy in patients with complete atrioventricular block and preserved left ventricular systolic function. Heart Rhythm. 2016;13:2272-2278. 
8. Nazeri A, Massumi A, Rasekh A, Saaed M, Frank C, Razavi M. Cardiac resynchronization therapy in patients with right ventricular pacing-induced cardiomyopathy. Pacing Clin Electrophysiol. 2010;33:37-40.