Cover Story

Integrating His Bundle Pacing in Clinical Practice

John J. Lee, MD1 and Daniel Weitz, MD, FHRS2 
1Columbia University, Division of Cardiology at Mount Sinai Medical Center, Miami Beach, Florida; 2Division of Electrophysiology, Holy Cross Medical Group Cardiology Associates of Fort Lauderdale, Fort Lauderdale, Florida

John J. Lee, MD1 and Daniel Weitz, MD, FHRS2 
1Columbia University, Division of Cardiology at Mount Sinai Medical Center, Miami Beach, Florida; 2Division of Electrophysiology, Holy Cross Medical Group Cardiology Associates of Fort Lauderdale, Fort Lauderdale, Florida

Introduction

His bundle pacing (HBP) has emerged as a potential alternative to right ventricular apical pacing. HBP can achieve QRS morphology that is nearly identical to the native QRS, and there is a growing body of evidence that HBP may truly achieve physiologic pacing.1-4 In addition to replacing traditional RV apical pacing, HBP may emerge as an alternative for failed cardiac resynchronization therapy (CRT)4-5 and for prevention of right ventricular apical pacing-induced cardiomyopathy.6-9

We demonstrate two examples of HBP: 1) In the setting of failed LV lead placement, HBP successfully narrowed a wide left bundle branch block (LBBB) QRS morphology; 2) Treatment of atrial fibrillation and tachycardia-induced cardiomyopathy with AV node ablation in conjunction with HBP.

Case #1

A 70-year-old male with a history of dilated non-ischemic cardiomyopathy, an ejection fraction (EF) of 30%, chronic LBBB, QRS width of 168 msec, and NYHA class II heart failure symptoms on long-term, guideline-based medical therapy, presented for CRT-D implant. 

During the procedure, a suitable coronary sinus branch was not found secondary to diaphragm stimulation from one of the available veins and non-capture from the other vein. The decision was made to perform HBP using the SelectSecure 3830 lead (69 cm; Medtronic). Non-selective His bundle capture was achieved with significant narrowing of the QRS. The His bundle capture threshold was achieved at 2.5V at 0.4 msec with non-selective RV pacing below 1.5V at 0.4 msec. At three-month follow-up, threshold numbers were unchanged. 

Case #2

An 83-year-old male with past medical history of difficult-to-control atrial fibrillation with both slow and rapid ventricular response and newly worsening EF reduced to 45% thought to be secondary to tachycardia-induced cardiomyopathy, presented for AV node ablation and pacemaker implant. Given the history of reduced ejection fraction, the decision was made to place a His bundle lead (SelectSecure 3830, 69 cm, Medtronic) as well as a backup traditional RV lead in the right ventricular apical septum. The His bundle lead was connected to the atrial port, and the right ventricular lead was connected to the ventricular port. The pacemaker was programmed at DDD with an AV delay of 350 msec. Following His bundle and RV lead placement, AV node ablation was performed per routine using a non-irrigated 8 mm catheter. Immediately post procedure, the His bundle capture was increased from 2.0V at 0.4 msec to 6.5V at 1.0 msec. The next day, the threshold had returned to normal and was maintained at the three-month checkup.

Discussion

The first case demonstrates the feasibility of His bundle pacing to eliminate LBBB in a patient with non-ischemic cardiomyopathy. If reverse remodeling ensues, the patient may have been spared epicardial lead placement. It is proposed that HBP can correct chronic bundle branch block by recruiting dormant fibers and thereby creating longitudinal dissociation in the His bundle.10-12 Moreover, even when the main His trunk is diseased, a direct pacing stimulus can result in distal His bundle capture because of the potential creation of a virtual distal electrode.12 In this case, after the failed CS lead placement, we selected HBP as an alternative option. Many HBP trials defined a successful HBP as maintaining a narrow QRS or more than 20% narrowing of QRS if the patient already had a baseline BBB.4, 10-12

In the second case, direct His bundle pacing is used to avoid further deterioration of LV systolic function in a patient that required 100% pacing. Due to reported occasional deterioration of His bundle pacing capture thresholds,3-5,10-12 a traditional right ventricular lead was also placed. Programming DDD pacing with a long AV delay allowed the traditional RV lead to be used only in the event of non-capture from the His bundle lead. The initial increase in His bundle thresholds was likely due to local edema from the AV node ablation, which abutted the His bundle lead. Fortunately, it appeared the edema resolved within several hours and the His bundle threshold was acceptable. ν

Disclosures: The authors have no conflicts of interest to report regarding the content herein.   

References

  1. Scherlag BJ, Lau SH, Helfant RH, Berkowitz WD, Stein E, Damato AN. Catheter technique for recording His bundle activity in man. Circulation. 1969;39:13-18.
  2. 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.
  3. 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(2):305-312.
  4. Kaufmann MR, McKillop MS, Burkart TA, Panna M, Miles WM, Conti CR. His Bundle Pacing: Rebirth of an Important Technique for Pacing the Intrinsic Conduction System. Cardiovascular Innovations and Applications. 2018;3(1):61-71.
  5. Sharma PS, Dandamudi G, Herweg B, et al. Permanent His-bundle pacing as an alternative to biventricular pacing for cardiac resynchronization therapy: a multicenter experience. Heart Rhythm. 2018;15(3):413-420.
  6. Van Oosterhout MFM, Prinzen FW, Arts T, et al. Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall. Circulation. 1998;98:588-595. 
  7. Little WC, Reeves RC, Arciniegas J, Katholi RE, Rogers EW. Mechanism of abnormal interventricular septal motion during delayed left ventricular activation. Circulation. 1982;65:1486-1491. 
  8. Tse HF, Lau CP. Long-term effect of right ventricular pacing on myocardial perfusion and function. J Am Coll Cardiol. 1997;29:744-749. 
  9. Lee MA, Dae MW, Langberg JL, et al. Effects of long-term right ventricular apical pacing on left ventricular perfusion, innervation, function and histology. J Am Coll Cardiol. 1994;24:225-232.
  10. El-Sherif N, Amay-Y-Leon F, Schonfield C, 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. Scherlag BJ, El-Sherif N, Hope RR, Lazzara R. The significance of dissociation of conduction in the canine His bundle. Electrophysiological studies in vivo and in vitro. J Electrocardiol. 1978;11:343-354.
  12. Vijayaraman P, Naperkowski A, Ellenbogen KA, Dandamudi G. Electrophysiologic insights into site of atrioventricular block: lessons from permanent His bundle pacing. JACC Clin Electrophysiol. 2015;1(6):571-581.
/sites/eplabdigest.com/files/articles/images/weitz-8.pdf