Case Study

Atrioventricular Node Ablation Combined with His Bundle Pacing to Reverse Atrial Fibrillation-Induced Cardiomyopathy

Giovanni Coluccia, MD

Arrhythmia Center, Department of Cardiology, Ospedali del Tigullio; Lavagna (GE), Italy 

Giovanni Coluccia, MD

Arrhythmia Center, Department of Cardiology, Ospedali del Tigullio; Lavagna (GE), Italy 


His bundle pacing (HBP) represents the only true physiological way of stimulation in patients requiring ventricular pacing. The first studies on permanent HBP were mostly conducted in patients who were candidates for atrioventricular node ablation (AVNA) due to poorly tolerated atrial fibrillation (AF).1-3 Since then, HBP has been expanded to include patients with every pacing indication, and also recently in patients who need cardiac resynchronization therapy (CRT) given its ability to correct intraventricular conduction disturbances, either alone or in combination with left ventricular (LV) pacing.4-6 

There have been many papers published in the last few years about HBP and Purkinje system pacing, reflecting a revival of great interest in this field. Perspectives on future applications are also encouraging. 

At present, in patients with AV block in which pacing is expected in a high percentage (>40%) of the time, in the presence of LV systolic dysfunction (LV ejection fraction 36-50%), HBP is indicated by the latest American guidelines as an alternative to CRT to avoid the deleterious effect of the dyssynchronous contraction obtained with stimulation from the right ventricular apical or septal myocardium.7 

We present a case of a patient with heart failure (HF) related to high ventricular rate AF that caused a tachycardia-induced cardiomyopathy; the condition progressively improved after AVNA and HBP until substantial reversal during early follow-up. Details about our stepwise approach to the procedure are described with the hope of sharing this powerful treatment option with the EP community for patients with AF and HF. 

Case Description 

A 63-year-old male presented to the Emergency Department with dyspnea (NYHA Class III) and chest discomfort. Clinical history revealed cigarette smoking, chronic obstructive pulmonary disease, previous alcohol abuse, and, five months earlier, a hospitalization for heart failure in which echocardiography had shown moderate LV systolic dysfunction but no critical lesions had been found on coronary angiogram. Medical treatment had been optimized to the maximum tolerated doses of an angiotensin-converting-enzyme inhibitor, beta-blocker, and aldosterone inhibitor. 

On physical examination, a body mass index of 42 kg/m2 and signs of central and peripheral congestion were found, together with high-rate arrhythmia and mild hypotension. Electrocardiogram (ECG) showed AF with a high ventricular rate (about 180 bpm) in the absence of relevant intraventricular conduction disturbancies; non-sustained runs of monomorphic ventricular tachycardia were seen. Blood tests were unremarkable. On echocardiogram, severely depressed LV ejection fraction was noted, with moderate mitral regurgitation and signs of moderate pulmonary hypertension; left atrial volume was also severely increased. Transesophageal echocardiography excluded intracavitary thrombosis. Multiple attempts at electrical cardioversion were ineffective, even after 24-hour intravenous amiodarone administration. Intravenous diuretics were necessary to improve the patient’s symptoms and recover from congestion, but a high ventricular rate (>160 bpm) persisted, even during treatment with amiodarone and then digoxin as adjuncts to the ongoing medical therapy. Considering the patient’s comorbidities and the very limited chances of maintaining long-term sinus rhythm, even despite likely multiple substrate ablation procedures, we offered the patient a strategy of rate control by means of AVNA and defibrillator (ICD) implantation, including HBP. 

During the procedure, baseline ECG and intracavitary electrograms showed a ventricular rate of about 170 bpm, QRS duration of 100 ms, and HV interval of 42 ms (Figure 1). After implanting the single-coil ICD lead in the distal portion of the interventricular septum, the HBP lead was screwed in (Figure 2) and selective capture was obtained with a bipolar threshold of 1 V at 0.5 ms pulse width, nonselective with a bipolar threshold of 4 V at 0.5 ms (Figure 3). Myocardial-only capture was not observed. Sensing resulted in an R wave of 0.5 mV. AVNA was performed during the same procedure, obtaining complete block with a single radiofrequency application quite far from the lead tip (Figure 4). The HB lead was connected to the atrial port of a dual-chamber ICD, and DDDR 85 ppm mode (AV delay 120 ms) was programmed. Electrical measurement remained stable after ablation, and ECG showed persistent selective HB capture. At one-month device follow-up, lead parameters were good, the rate was reduced to 75 ppm, and atrioventricular block persisted with a Hisian escape rhythm around 50 bpm. At three-month follow-up, the patient’s exercise capacity was good in the absence of relevant limitations due to effort dyspnea (NYHA Class I-II). On echocardiography, LV ejection fraction had markedly improved from 28% to 48%, no signs of pulmonary hypertension were seen, and mitral regurgitation was mild. HB lead position appeared to be just above the septal leaflet insertion of the tricuspid valve (Figure 5).


Among patients with HF, permanent AF, and narrow QRS, AVNA plus CRT has been demonstrated to be beneficial compared with medical therapy in terms of reduction of HF hospitalization and improvement in quality of life.8 HBP is expected to present similar or even better outcomes, allowing maintenance of physiological electrical activation of the ventricles. 

The ablate-and-pace procedure, in the case of HBP, is performed in three steps at our center. First, we implant the ventricular lead (ICD lead or backup lead) and the HB lead, taking care to target the distal HB. The His potential is mapped with the HBP lead (SelectSecure, model 3830, 69 cm, Medtronic), delivered through a fixed-curve or deflectable sheath (C315His or C304 SelectSite, Medtronic), and advanced from the left axillary vein. A unipolar connection is used to record a HB potential on the lead tip and the catheter is fixed in that position, provided it presents good capture threshold; after fixation, a HB wave is required to still be recorded and the presence of a current of injury is carefully evaluated. HB selective and nonselective (and with or without bundle branch block correction, if appropriate) capture thresholds are assessed and considered acceptable if not superior to 2.5 V at 1 ms pulse width.9 When the HB-paced QRS remains wide without bundle branch block correction (if present at baseline), an LV lead is also implanted via the coronary venous system, targeting lateral vessels. 

The second step is to perform radiofrequency AVNA. An ablation catheter (usually a non-irrigated, 4 mm tip) is advanced from the right common femoral vein to the right atrium, and ablation usually starts at a site corresponding to the radiological projection of the anodal ring of the HBP lead, as far as possible from the tip.3 If necessary, further radiofrequency applications are performed cranially, towards the lead tip, until complete block is observed. Successful ablation sites generally present electrograms showing a 1:1 ratio between atrial and ventricular signals, in absence of HB potential. Once AV block is obtained, the characteristics of the escape rhythm are evaluated (especially to assess if an HB potential is still present on the pacing lead), as well as the types of HB capture, and electrical measurements are repeated to verify unchanged values. 

After ten minutes of persistent AV block, the third step is to remove the HB delivery sheath, fix the leads, connect them to the device, and close the pocket. In this phase, special care is made to give appropriate slack to the HBP lead in order to avoid dislodgements. Connections are made according to the advice by Burri et al10: in cases of permanent AF, the atrial port is usually used for the HBP lead. Device programming depends on connections; when the HBP lead is in the atrial port and HB is desired as the only pacing site, DDDR mode is generally used and AV delay is programmed 20-40 ms greater than the measured interval between the “atrial pace” and “ventricular sense” events of the device telemetry. We often provide patients with remote monitoring devices and set an alarm when the ventricular pacing percentage becomes greater than 5%, likely indicating a corresponding loss of HB capture or a need to reprogram the AV delay. 


This case confirms that HBP can provide a unique way to preserve physiological ventricular electrical activation, which is particularly important in patients presenting with normal His-Purkinje conduction at baseline and an indication to AVNA, where 100% pacing is desired. It is likely that the growing interest in physiological pacing and the ongoing technological advancements in this field will soon revolutionize the way we approach cardiac pacing. 

Disclosure: Dr. Coluccia has no conflicts of interest to report regarding the content herein.

Editor’s Note: This article underwent peer review by one or more members of EP Lab Digest’s editorial board.

For more information, please contact the author on Twitter at @messapus

  1. 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.
  2. Occhetta E, Bortnik M, Magnani A, et al. Prevention of ventricular desynchronization by permanent para-Hisian pacing after atrioventricular node ablation in chronic atrial fibrillation: a crossover, blinded, randomized study versus apical right ventricular pacing. J Am Coll Cardiol. 2006;47:1938-1945.
  3. Vijayaraman P, Subzposh FA, Naperkowski A. Atrioventricular node ablation and His bundle pacing. Europace. 2017;19:iv10-16.
  4. Abdelrahman M, Subzposh FA, Beer D, et al. Clinical outcomes of His bundle pacing compared to right ventricular pacing. J Am Coll Cardiol. 2018;71:2319-2330.
  5. Vijayaraman P, Herweg B, Ellenbogen KA, Gajek J. His-optimized cardiac resynchronization therapy to maximize electrical resynchronization. Circ Arrhythm Electrophysiol. 2019;2:e006934.
  6. Coluccia G, Vitale E, Corallo S, et al. Additional benefits of non-conventional modalities of cardiac resynchronization therapy using His bundle pacing. J Cardiovasc Electrophysiol. 2020 Jan 19. 
  7. Kusumoto FM, Schoenfeld MH, Barrett C, et al. 2018 ACC/AHA/HRS Guideline on the evaluation and management of patients with bradycardia and cardiac conduction delay: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. Circulation. 2019;140(8):e382-e482.
  8. Brignole M, Pokushalov E, Pentimalli F, et al, APAF-CRT Investigators. A randomized controlled trial of atrioventricular junction ablation and cardiac resynchronization therapy in patients with permanent atrial fibrillation and narrow QRS. Eur Heart J. 2018;39(45):3999-4008.
  9. Vijayaraman P, Dandamudi G, Zanon F, et al. Permanent His bundle pacing: recommendations from a multicenter His bundle pacing collaborative working group for standardization of definitions, implant measurements, and follow-up. Heart Rhythm. 2018;15:460-468.
  10. Burri H, Keene D, Whinnett Z, Zanon F, Vijayaraman P. Device programming for His bundle pacing. Circ Arrhythm Electrophysiol. 2019;12:e006816.