Implanting a Permanent His Bundle Pacemaker: The Indiana University Approach

Introduction

Activation of the intrinsic His-Purkinje system (HPS) allows for a highly synchronized contraction of ventricular tissue in humans. This efficient activation is disrupted during artificially paced rhythms. Over the years, conventional pacing from the right ventricular apex (RVA) has been associated with heart failure (HF), increased atrial fibrillation (AF), and mortality.^1,2 Biventricular (BiV) pacing has emerged as a potentially superior form of pacing. It can be technically challenging and has its shortcomings as well, including an inability to achieve clinically successful outcomes in one-third of patients who undergo the procedure. His bundle pacing (HBP) is a physiological form of ventricular pacing (VP) that preserves atrioventricular and ventricular synchrony. Permanent HBP was first described in 2000, after Deshmukh et al published good outcomes in patients with chronic AF who underwent AV nodal ablation and HBP.³ Over the past few years, there has been an increasing usage of HBP in routine clinic practice, primarily due to the potential for achieving 100% electrical synchrony and to possibly reduce HF incidence from long-term pacing.^4-7 Furthermore, HBP has led to successful resynchronization in patients with chronic LBBB.^8,9 We present a recent case where permanent HBP was successfully achieved, and briefly describe some technical aspects related to this form of pacing. 

Case Description

A 62-year-old female, with a history of an atrial septal defect repair at age 5, underwent tricuspid valve (TV) repair with a ring placement for severe tricuspid regurgitation at age 53. She also had persistent AF treated with warfarin (Figure 1). She would experience periods of symptomatic junctional bradycardia (despite no AV nodal drugs), and was referred for permanent pacemaker implantation. Options were discussed, and after careful consideration, she consented to undergo permanent HBP. 

On the day of the procedure, she was found to be in atrial flutter (Figure 2). After a left pectoral subcutaneous pocket was created, left axillary vein access was obtained using the modified Seldinger technique. Through a short 7 French sheath, a C315 His fixed-curve sheath (Medtronic) was advanced over a J-wire into the right atrium. A 69 cm 3830 bipolar pacing lead (Medtronic) was then advanced through the sheath, and the lead tip was slightly exposed outside the sheath. The entire apparatus was then advanced in a gentle clockwise motion to the tricuspid annulus. The patient had a C-ring with the septum exposed, and His bundle (HB) mapping was performed in a unipolar configuration (distal electrode and skin). HB recordings were obtained using a sweep speed of 100 mm/s for easier detection (both the pace-sense analyzer and EP recording system were used in this case) (Figure 2). Unipolar pacing was performed using the distal pole of the lead starting at 5V @ 1 ms and assessing 12-lead QRS morphologies (Figure 3). At higher pacing outputs (up to 1.25V @ 1 ms), non-selective His bundle pacing (NSHBP, defined as stimulus to QRS interval shorter than intrinsic HV interval from the same site and local fusion demonstrated on a 12-lead ECG) was seen. Selective His bundle pacing (SHBP, defined as the stimulus to ventricular activation equal to the intrinsic HV interval and paced QRS morphology identical to the intrinsic QRS complex) was seen at lower outputs (up to 0.5V @ 1 ms). 

The lead was then turned 5-6 times in a clockwise fashion, and torque transmission was confirmed via tactile sensation. Excellent NSHBP was seen at the final implant programmed output of 3.5V @ 1 ms (Figure 4). An atrial lead was advanced through a 7F sheath into the posterolateral RA (where acceptable P waves were encountered) and screwed into place with good current of injury. An Adapta L device (Medtronic) with RA lead (Model 5076, 52 cm, Medtronic; sensing at 0.8 mV, impedance of 530 ohms, atrial flutter) and RV lead (Model 3830, 69 cm, Medtronic; sensing at 6.0 mV, impedance at 594 ohms, SHBP threshold at 0.5V @ 1.0 ms) was implanted in this patient. Brady parameters were set at DDDR 60-120 bpm with a paced/sensed AV delay of 120/120 ms to account for intrinsic HV delay. A chest x-ray the following morning showed the His lead location (Figure 5). 

She was admitted for dofetilide loading and converted to normal sinus rhythm the following morning. She was discharged home with no issues 3 days later.

Discussion

Over the years, HBP has been shown to be safe and feasible as a permanent form of VP in observational as well as small randomized trials.^4,6,8,10 It has been performed safely and effectively even in patients with complete nodal and infranodal block.^6,11 It has been shown in a small randomized trial to be a viable alternative to biventricular pacing in patients with chronic LBBB and symptomatic HF.⁸ HBP may lead to a reduced incidence of pacing-induced HF and even reverse chronic RV pacing-induced cardiomyopathy.¹² 

The procedure does require some experience in using the fixed-curve C315 His sheath and anchoring the lead, which has an exposed helix (solid core lead with inability to use an inner stylet). An alternative deflectable sheath (C304, Medtronic) is also available and can be useful at times in difficult anatomies. The tissue being stimulated (His bundle) is intrinsically different than the conventional RV endocardium and LV epicardium. Careful attention to detail, such as HB recordings, subtle changes in QRS morphology during pacing, sensing margins, and pacing thresholds need to be carefully reviewed intraprocedurally as well as during follow-up.¹³ Detailed atrioventricular bundle anatomy in humans has been well characterized, and its understanding is crucial to safely and successfully perform HBP in clinical practice.14,15 In brief, there are three described anatomical variations to the HPS: Type I, where the AV bundle runs along the lower border of membranous septum and is covered with a thin layer of myocardial fibers; Type II, where the AV bundle is discretely separated from the membranous septum and insulated by thick fibers; and Type III, where the AV bundle is naked and runs beneath the endocardium with no insulation. Type I anatomy may explain the transition from NSHBP to SHBP, as the pacing output is reduced (as seen in our case); at higher output, the tissue surrounding the thinly insulated HB is also being recruited, leading to a fused QRS. In Type II anatomy, variable fusion may be present at all outputs (NSHBP), and in Type III anatomy, SHBP can be easily demonstrated at varying pacing outputs. 

In our opinion, there is a steep learning curve related to the limited availability of tools and variable patient anatomies. We recommend that early procedures be aimed at patients with sinus node dysfunction who are not ventricular pace-dependent (but a RV lead is placed) until appropriate experience is gained. The procedure can also be attempted in patients with LBBB who fail a traditional cardiac resynchronization therapy approach with an LV lead prior to referral for surgical LV lead placement. 

Conclusion

Permanent HBP can be safe and effective, and lead to improved outcomes in patients requiring VP. Successful implementation in practice requires detailed understanding of the anatomy and physiology of the HB, and appreciating various pacing responses as outlined above. With further randomized studies showing improved outcomes and better tools (leads and delivery mechanisms), we firmly believe that permanent HBP will become a common form of VP in the near future.

Disclosures: Dr. Maatman has no conflicts of interest to report regarding the content herein. Dr. Dandamudi reports he is a consultant for Medtronic, Inc.

References

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