Atrioventricular nodal ablation (AVNA) represents a critical intervention in the management of refractory atrial fibrillation (AF) and heart failure (HF). When combined with biventricular pacing or conduction system pacing, particularly His bundle pacing and left bundle branch area pacing, this strategy offers distinct and complementary benefits. While each pacing modality presents unique advantages and potential limitations, their combination with AVNA offers a comprehensive and individualized treatment strategy for addressing associated HF. This integrated approach can enhance symptom control, improve hemodynamic performance, and contribute to better long-term outcomes in patients with advanced HF and AF.
Key points
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Atrioventricular nodal ablation and pacing should always be considered as a therapeutic option in refractory atrial fibrillation and heart failure.
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In patients undergoing this strategy, achieving close to 100% pacing is essential to optimize outcomes.
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This can be accomplished through cardiac resynchronization therapy or conduction system pacing, including His bundle pacing and left bundle branch area pacing.
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Careful consideration of patient-specific factors is critical when selecting the most appropriate pacing modality to maximize therapeutic benefits and minimize risks.
Introduction
Atrial fibrillation (AF) and heart failure (HF) frequently coexist, with each condition exacerbating the other. AF can precede or follow both HF with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF), contributing to HF progression and begetting persistence of persistent AF. This, in turn, leads to further cardiac structural and functional changes, creating a vicious cycle. Epidemiologic studies indicate that 24% to 44% of patients with acute HF and 33% of patients with chronic HF present with AF. Animal models of persistent atrial tachycardia, induced by rapid right atrial appendage pacing, demonstrate decreased left ventricular (LV) contractility, reduced myocardial blood flow, and increased LV wall stress. These changes involve complex remodeling of tissue, myocyte, and ionic channel including fibrosis, extracellular matrix disarray, increased apoptosis, and alterations in calcium handling.
Optimizing medical therapy for HF and LV systolic dysfunction typically involves beta-blockers, angiotensin receptor-neprilysin inhibitors (ARNIs)/angiotensin-converting enzyme inhibitors (ACEIs)/angiotensin receptor blockers (ARBs), sodium-glucose cotransporter-2 inhibitors (SGLT-2), diuretics, and aldosterone antagonists to promote reversal of remodeling. However, despite advancements in pharmacologic treatments, challenges in efficacy persist. The most effective way to interrupt the vicious cycle between AF and HF is to restore sinus rhythm. Catheter ablation prevents AF recurrences, reduces AF burden, and improves quality of life in symptomatic paroxysmal or persistent AF (PeAF) who are intolerant or do not respond to antiarrhythmic drugs (AADs). Several randomized trials, including CASTLE-AF, CAMERA-MRI, and AMICA, have demonstrated that successful catheter ablation of AF in patients with HFrEF significantly reduces arrhythmia recurrence, increases ejection fraction (EF), and improves clinical outcomes and survival. However, AF recurrence following the rhythm-control strategy remains high particularly in patients who developed atrial and ventricular fibrosis. Moreover, the benefits of AF ablation in patients with HFpEF are less well-established compared to those with HFrEF.
Atrioventricular nodal ablation
Anatomy of Atrioventricular Node
The atrioventricular (AV) node is a compact spindle-shaped structure connected to the His bundle. In adults, it measures approximately 5.0 mm in length, 5.0 mm in width, and 0.8 mm in thickness. Located within the triangle of Koch, defined by the tendon of Todaro, the septal leaflet of the tricuspid valve, and the floor of the coronary sinus ostium ( Fig. 1 ).
Technical Consideration
AV nodal ablation (AVNA) is considered when AF results in a rapid ventricular rate despite aggressive catheter ablation and adequate AV nodal blocking drugs or when such drugs are ineffective, contraindicated, or poorly tolerated. First performed in humans in 1981, AVNA is relatively straightforward but renders patients pacemaker-dependent. Complete AV block can be successfully achieved by a right-sided ablation approach in 95% to 97% of patients.
The procedure typically employs radiofrequency energy via right femoral vein access, with ablation lesions guided by intracardiac electrograms. The goal is to preserve automaticity and conduction distal to the ablation site, achieving complete AV block with a stable junctional escape rhythm. Three-dimensional electroanatomic mapping (3D-EAM) can aid in locating the AV node and His bundle. The presence of rapid junctional rhythm can be a precursor of complete AV block. A more superior ablation point should be considered in case of failure at the initial site. When His bundle pacing (details in later discussion) is performed prior to AVNA, the His pacing lead can be used as a marker to locate optimal site for AVNA. Operators initially target the AV node inferiorly and posteriorly to the His bundle lead tip at or below the ring electrode level ( Figs. 2 and 3 A ). In order to avoid compromising His bundle pacing thresholds following AVNA, a starting lower power should be performed with His bundle pacing. An ideal location for ablation is identified by recording a large atrial electrogram with a ventricular electrogram and a non-QS morphology of unipolar His potential. Prior to ablation pacing fom the His lead at 0.5V/0.4 ms above the threshold should be initiated. Once loss of His activation capture is detected, ablation should be immediately suspended to avoid further threshold rise. After complete AV block is achieved, it is advisable to wait for at least 15 minutes to evaluate AV conduction recovery. Additional applications may be applied close to the successful lesion as necessary.
A common pitfall of AVNA is applying radiofrequency lesion at sites with a right bundle potential. The most common per-procedural predictor of AVNA failure is the inability to record a definite His potential, which can be challenging in patients with AF. In some cases, ablation failure is due to multiple ineffective RF deliveries that can cause progressive development of edema and swelling around the region of the AV node. In less than 5% of cases, particularly in patients with structural heart disease or prior failed ablations, a left-sided approach via retrograde aortic access may be necessary. ,
Pacing therapy
Non-conduction System Pacing
Following AVNA, permanent pacing is required for adequate heart rate support. Initially, right ventricular (RV) pacing was commonly employed, and the pacing lead is usually implanted in RV apex or RV septum. The AIRCRAFT trial demonstrated that AVNA combined with RV pacing improved quality of life in PeAF patients with severe symptoms or drug refractoriness compared to AADs alone.
However, RV pacing is suboptimal for patients with HF, particularly those with HFrEF, due to the nonphysiological, dyssynchronous activation of the cardiac chambers. Long-term RV pacing can lead to regional wall motion abnormalities and adverse LV hemodynamics related to pacing-induced dyssynchrony. While cardiac resynchronization therapy (CRT) achieves biventricular pacing (BVP) by adding an LV pacing lead ( Fig. 3 B), this method has certain disadvantages such as diaphragm stimulation, high threshold, and risks of LV electrode dislodgment/loss of capture, and 30% to 50% of cases showing nonresponsiveness to BVP. Successful CRT delivery with effective BVP in the setting of AF is challenging, and if not achieved, many patients will simply not respond. Furthermore, device interrogation may suggest a higher ventricular pacing percentage in patients with AF, but fusion beats or pseudofusion beats may represent a significant portion of ventricular pacing. This dilemma is largely solved in patients receiving CRT with AF who underwent AVNA.
Evidence for biventricular pacing
The PAVE study first introduced the concept of “ablation and pacing,” demonstrating improved LV EF and HF symptoms with CRT in patients with reduced EF. Subsequent randomized controlled trials comparing BVP to RV pacing after AVNA have consistently shown increased LVEF, decreased LV end-systolic volume, and functional improvement. The RESPONSIBLE trial evaluated fixed-rate versus rate-responsive pacing in patients with permanent, refractory AF and LV dysfunction treated with AVNA and CRT. Results indicated that rate-responsive pacing significantly improved exercise capacity in PeAF patients with uncontrolled rates and reduced LVEF who had undergone AVNA and BVP.
More recently, the APAF-CRT trial demonstrated a survival advantage in narrow QRS patients undergoing AVNA with BVP compared to standard care. These findings have led to the re-emergence of “ablate and pace therapy” as a potential first-line treatment of those patients with AF of a long-standing and permanent nature. Importantly, the heart rate at enrollment was less than 110 bpm in both arms, which suggests that reversing irregulopathy is the leading mechanism of benefit rather than tachycardia. Additionally, the atrial kick is not restored in ablate and pace strategies, yet improved survival was observed in a trial of 133 patients.
The success of this approach supports the hypothesis that rendering patients pacemaker-dependent ensures appropriate CRT delivery. An additional benefit of CRT in patients with AF is the potential for spontaneous reversion to sinus rhythm, particularly within the first few months after implantation. Factors associated with this reversion include smaller LV end-diastolic diameter, shorter post-CRT QRS duration, smaller left atrial diameter, and AVNA. Notably, due to maintenance of biventricular synchronization and restoration of atrio-ventricular synchronization, patients experiencing spontaneous return to sinus rhythm demonstrated an 87% reduction in 1 year mortality.
Based on these findings, CRT is recommended after AVNA in patients with LVEF less than 45%. For those with existing RV pacing systems, CRT should be considered if EF is reduced. However, high-quality evidence supporting CRT benefits in AF patients with HFpEF remains limited.
Conduction System Pacing
Recent advancements have led to the development of conduction system pacing (CSP) options, namely left bundle branch (LBB) area pacing (LBBAP) and His bundle pacing (HBP). These approaches allow for more physiologic activation of the cardiac chambers and myocardium, potentially preserving LV function ( Fig. 3 C, D). It is anticipated that the benefits observed with BVP are likely to be further amplified with CSP due to the preservation of intrinsic ventricular activation sequence.
His bundle pacing
Anatomy of His Bundle
The His bundle is a 20 mm long, cord-like ventricular structure, about 4 mm in diameter, extending from the AV node and penetrating the membranous interventricular septum (IVS). The His bundle, encapsulated by fibrous tissue in the membranous septum, originates from the primitive IVS. During fetal development, it connects with the AV node in the second trimester. Recent anatomic studies have identified 3 common His bundle variations: type I: runs along the lower membranous IVS border, covered by thin myocardial fibers; type II: separated from the lower muscular septum border; and type III: exposed, lying directly beneath the endocardium on the membranous IVS. Anomalous left-sided courses have also been observed. These anatomic variations impact selective HBP and may explain transient or persistent conduction disturbances. Both atrial and ventricular portions of the His bundle are accessible for permanent ventricular pacing. Understanding these variations is crucial for successful HBP implementation and interpreting potential complications in clinical practice.
Technical Considerations
Deshmukh and colleagues pioneered permanent HBP in patients with AF, demonstrating its potential to enhance cardiac function. HBP, a physiologic pacing method, involves inserting an electrode into the His bundle to promote cardiac resynchronization and improve clinical outcomes. The procedure utilizes unipolar potential mapping with continuous intracardiac electrogram recording. His bundle localization is facilitated by imaging the tricuspid valve annulus using contrast angiography or 3D-EAM. The pacing lead is advanced to the His bundle area, identified by larger ventricular and smaller atrial signals (atrial/ventricular electrogram ratio ≥1:2). Specialized equipment, including the SelectSecure 3830 lead and C315His or C304 SelectSite sheaths (Medtronic, US), has made HBP feasible in routine clinical practice. The lead is screwed into position, with a threshold of 2 V or less at 1 millisecond pulse width being considered appropriate. His bundle injury current, recorded in 40% of patients, requires adjusting the high-pass filter to 0.5 Hz. In His-Purkinje conduction disease (HPCD), higher capture thresholds may be acceptable if the RV capture threshold is significantly lower. Mapping the distal His bundle beyond intra-Hisian block is crucial for achieving low capture thresholds in these cases.
The operators should also distinguish the selective HBP (only captured by the pacing stimulus), and nonselective HBP (fusion capture of the His bundle and adjacent ventricular tissues). Criteria for selective HBP include (1) S-QRS interval equals H-QRS interval (may be shorter in HPCD), (2) discrete local ventricular electrogram from pacing artifact, (3) paced QRS morphology matches native QRS (may be narrower in HPCD), and (4) single capture threshold observed ( Fig. 4 ).
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