Review Article

Determining Good Candidates for Atrioventricular Junction Ablation and Device Therapy and Which Device to Implant

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Abstract

The ‘ablate-and-pace’ strategy, combining atrioventricular junction ablation with permanent pacing, has re-emerged as a valuable therapeutic option for patients with AF who are symptomatic, have poor rate control or develop AF-mediated cardiomyopathy. While historically considered a last-resort treatment, recent randomised trials and meta-analyses support its efficacy in improving functional status, reducing hospitalisations and potentially enhancing survival, particularly when paired with CRT or conduction system pacing. The success of this approach depends on careful patient selection and appropriate device choice. Candidates include patients with uncontrolled ventricular rates, tachycardia–bradycardia syndrome, symptomatic bradycardia or those with poor CRT response due to persistent AF. Right ventricular pacing should be avoided when possible, in favour of biventricular or conduction system pacing, which preserves synchrony and reduces pacing-induced cardiomyopathy. This review discusses clinical scenarios, prognostic considerations, and current device options – including leadless systems – offering a practical guide for tailoring atrioventricular junction ablation-based therapies to individual patient profiles.

Keywords

Atrioventricular junction ablation, AF, heart failure, cardiac resynchronisation therapy, conduction system pacing,

Received:

Accepted:

Published online:

DOI: https://doi.org/10.15420/aer.2025.41

Disclosure: AB has received consulting fees and honoraria from AstraZeneca, Bayer, BMS/Pfizer, Medtronic, Vifor Pharma and Alnylam. TL has received consulting fees from Bayer, BMS/Pfizer, Boehringer Ingelheim and Novo Nordisk and honoraria from AstraZeneca, Boston Scientific, Medtronic and Novo Nordisk. All other authors have no conflicts of interest to declare.

Correspondence: Laurent Fauchier, Service de Cardiologie, Centre Hospitalier Regional Universitaire et Faculté de Médecine de Tours, 2 Boulevard Tonnellé, 37000 Tours, France. E: laurent.fauchier@univ-tours.fr

Copyright:

© The Author(s). This work is open access and is licensed under CC-BY-NC 4.0. Users may copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Atrioventricular (AV) junction ablation (AVJA) combined with permanent pacing – commonly referred to as the ‘ablate-and-pace’ strategy – has emerged as a therapeutic option in selected patients with AF, particularly those with heart failure (HF) or poor rate control despite optimal medical therapy.1 Beyond its historical use in controlling tachycardia, AVJA may alleviate the deleterious effects of RR interval irregularity (irregulopathy) and improve cardiac function in AF-related cardiomyopathy. The clinical benefit of AVJA depends not only on patient selection but also on the pacing modality employed, with growing interest in biventricular pacing (BiVP) and conduction system pacing (CSP) as alternatives to right ventricular pacing (RVP). In this review, we examine the pathophysiological rationale for AVJA in AF and HF, clinical indications and patient selection, and current options for device therapy – including transvenous and leadless systems – when AVJA is needed.

Pathophysiological Rationale for Atrioventricular Junction Ablation in AF With Heart Failure

AF is often associated with either HF with reduced ejection fraction (HFrEF) or with preserved ejection fraction (HFpEF). These two conditions coexist in approximately 50% of patients.2 AF may induce HF by increased heart rate corresponding to the so-called ‘tachycardia-induced cardiomyopathy.’ AF may also induce HF in patients with adequate rate control by irregular beat-to-beat intervals in cases of AF-induced cardiomyopathy, also called irregulopathy.3

Tachycardia-induced Cardiomyopathy

Tachycardia-induced cardiomyopathy is defined as a reversible form of dilated cardiomyopathy with left ventricular (LV) dysfunction mostly caused by chronically elevated ventricular rates, in the context of AF or any other arrhythmia.3,4 Several mechanisms are proposed to explain the occurrence of such cardiomyopathies in the context of persistent tachycardia.

In animal models, experimental tachycardia-induced cardiomyopathy has been described for over 50 years, mainly in pigs and dogs.5 These animal models constitute a solid basis for the pathophysiological understanding of this specific entity. Sustained rapid atrial or ventricular pacing in animal models has been shown to induce severe biventricular systolic and diastolic dysfunction, with severe reduction of cardiac output and elevated systemic vascular resistance, typically with marked LV dilatation without LV hypertrophy.6 Systolic dysfunction in tachycardia-induced cardiomyopathy is coupled with diastolic dysfunction, both at the organ and cellular levels.7,8 The incomplete relaxation leaves cardiomyocytes in a constant activated state called diastolic contracture.9 This leads to elevated wall pressures, which may be responsible for observed decreased myocardial blood flow in chronic supraventricular tachycardia, further worsening cardiac dysfunction.10 This also leads to a neurohormonal activation, notably of the renin–angiotensin–aldosterone axis, and elevated epinephrine and norepinephrine levels.11 Extensive structural remodelling has also been described, affecting both myocytes and extracellular matrix, compromising myocyte alignment and subsequent coupling, mechanical and electrical.12 This remodelling and change in cardiomyocyte morphology is associated with macrophage-dominated cardiac inflammation.13

Among the alterations affecting myocytes, depletion of T-tubules, associated with decreases in the density of L-type calcium channel currents and β-adrenergic receptors, is of particular importance.4 Indeed, at a cellular level, the loss of myocardial contractility and contractile reserve may be at least partly explained by a reduced β1-receptor density at the cellular surface, associated with perturbations in the post-receptor adenylate cyclase and calcium handling.14,15 A blunted response to β-adrenergic stimulation in these models has been largely described, and plays a role in the systolic dysfunction.16–18 Abnormalities in calcium handling, such as reduced calcium transients and L-type calcium current through calcium channels and sarcoplasmic reticulum calcium transport are correlated with the severity of ventricular dysfunction, as they result in impaired excitation–contraction coupling through a variability in the time course activation of cardiomyocytes, finally altering contraction efficiency.4,19,20 Abnormalities in calcium handling are also responsible for diastolic dysfunction, as tachycardia induces an increase in sarcoplasmic reticulum calcium content, causing calcium extrusion via the sarcolemmal sodium–calcium exchanger in a high calcium cytosol and subsequently impairing cardiomyocyte relaxation.21 Chronic tachycardia also induces myocardial energy depletion, notably of high-energy phosphates, with an impairment of energy metabolism in cardiomyocytes.20,22 The increased metabolic burden leads to an overload of oxidative metabolism in cardiac mitochondria, with subsequent ATP depletion and mitochondrial dysfunction, concurring with an overall oxidative stress participating in contractile dysfunction.22–24

Additionally, rapid atrial pacing also induces an atrial cardiomyopathy, with similar systolic and diastolic dysfunction, atrial enlargement, abnormalities in calcium handling and in energy metabolism.25,26 These abnormalities are generally reversible a few weeks after cessation of chronic tachycardia. However, in patients in whom durable restoration of sinus rhythm is not achievable, these tachycardia-induced mechanisms suggest that rate control strategies may produce at least some benefit in patients with such cardiomyopathies.

Heart Failure beyond Tachycardia: AF-induced Cardiomyopathy

Beyond tachycardia-induced cardiomyopathy, HFrEF has also been described in patients with AF with adequate rate control, leading to the emergence of the concept of AF-induced cardiomyopathy.3

The mechanism underlying AF-induced cardiomyopathy is still unclear, but several mechanisms are suspected, often like those underlying HFpEF in patients with AF. Indeed, HFpEF is also frequent in patients with AF and, although the pathophysiology behind this association remains uncertain, many elements are known to induce HF in such patients.27,28 Among these mechanisms, common elements are systemic and atrial inflammation, excessive oxidative stress and altered energy metabolism, along with electrical and structural remodelling involving epicardial adipose tissue leading to left-atrial remodelling and fibrosis.29,30

AF-induced cardiomyopathy shares some suspected mechanisms with those already discovered in HFpEF.31 Indeed, as in tachycardia-induced cardiomyopathy and HFpEF, abnormalities in calcium handling and dynamics appear to play an important role, perhaps originating in the irregularity of RR intervals.3 The loss of atrial systole – and therefore of both its contractility and emptying – is also suspected to participate in an increased sympathetic activation and impaired ventricular filling, ultimately leading to a diastolic and finally systolic dysfunction.32

At the cellular level, atrial mitochondrial dysfunction is also prevalent in these patients, suggesting that energy depletion and metabolic dysregulation with excessive oxidative stress might also have a role in the development of HF.33

Finally, the mere irregularity of ventricular cycle lengths might be a determinant of HF in patients with AF. Indeed, it has been demonstrated that pacing with an irregular sequence of RR intervals decreases cardiac output and increases intracardiac pressures when compared with a same-rate regular sequence of RR intervals, illustrating the fact that cycle length irregularity in itself may produce adverse haemodynamic effects.34 Variability in cycle length produces varying LV systolic performances in AF, with reduction of stroke volume during short intervals not fully compensated by the long intervals, as the Frank-Starling mechanism doesn’t apply for such intervals.35 Therefore, the irregularity of RR intervals in AF is key in the development of HF. It is important to note that the degree of ventricular irregularity (i.e. the dispersion of RR intervals) is not only the consequence of AF activity, but mainly of the conductivity within the AV junction. Put differently, while AF is responsible for the random character of the RR interval, the degree of ventricular irregularity lies in the AV junction.36

Considering these elements, if rate control might not be sufficient in patients with AF, a radical strategy of AVJA with implantation of a permanent pacemaker would appear potentially beneficial in selected patients, acting both on tachycardia-induced pathophysiological elements and on ventricular irregularity. However, this strategy results in the shift of AF towards permanent AF in almost one-third of patients within 2 months, with subsequent progression towards atrial cardiomyopathy as mentioned previously.4 The choice of this strategy would also be made at the cost of potential complications associated with transvenous pacemakers and of the risk of pacing-induced cardiomyopathy in pacing-dependent patients.

Indications and Patient Selection for Atrioventricular Junction Ablation

The management of patients with AF includes rate control and rhythm control strategies.1 The choice between these two strategies as a first line has been a matter of debate for a long time, since the evidence showing superiority of rhythm control on rate control is very recent.37 Consequently, rate control may be preferred over rhythm control for elderly, frail and comorbid patients given the extensive adverse effects associated with antiarrhythmic medications. Rate control can also be used in patients who have failed rhythm control strategies, including ablation or electrical cardioversion, especially in those in whom catheter ablation yields modest efficacy or pharmacological agents are poorly tolerated, such as patients with hypertrophic cardiomyopathy and cardiac amyloidosis. The traditional method of rate control is using AV nodal blocking agents, but their use can be limited by patient general intolerance, hypotension or inefficacy to reduce heart rate. Since its first description in 1982, the method for AVJA has evolved and has been shown to be an effective option to achieve a very strict and stable heart rate control.38,39 Compared with drug treatment, AVJA has been associated with a lower risk of mortality in a large registry and improvement in symptoms and quality of life, with a low incidence of procedure morbidity in a meta-analysis.40,41 The pace-and-ablate strategy is therefore routinely performed to control heart rate and reduce symptoms in patients unresponsive or intolerant to intensive rate and rhythm control therapy, or who are ineligible for AF ablation, accepting that these patients will become pacemaker-dependent (Figure 1 ).1,42–44 A class 2a indication is provided in the 2024 European Society of Cardiology (ESC) guidelines on AF management for these patients.1

Figure 1: Indications of Atrioventricular Junction Ablation for the Treatment of AF According to Current Guidelines1,42–44

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Once AVJA is decided upon, the second crucial question about the pace-and-ablate strategy is: how to pace the patient? Indeed, despite improving LV ejection fraction (LVEF) in the majority of patients, AVJA associated with permanent RVP delays LV activation in ~50% of patients and can lead to a pacing-induced cardiomyopathy and consequently worse outcomes.45 BiVP may prevent RVP-induced LV dyssynchrony. Brignole et al. reported a significant reduction in mortality, quality of life and hospitalisation for heart failure (HFH) in elderly patients with symptomatic permanent AF and at least one HFH during the last year, who were treated with AVJA and BiVP compared with pharmacological heart rate control.46 It is therefore recommended that AVJA combined with BiVP should be considered in severely symptomatic patients with permanent AF and at least one HFH to reduce symptoms, physical limitations, recurrent HFH, and mortality (class 2a, level of evidence b).1 Alternatively, the 2023 Heart Rhythm Society/Asia Pacific Heart Rhythm Society/Latin American Heart Rhythm Society (HRS/APHRS/LAHRS) and 2025 ESC consensus statement on physiological pacing introduced the possibility of CSP including His bundle pacing (HBP) and left bundle branch area pacing (LBBAP) instead of BiVP in first intention in patients with LVEF ≥50% and in second intention after BiVP in patient LVEF <50% (class 2b).42,43 This proposition is based on several recent observational retrospective studies, showing non-inferiority in CSP outcomes compared with BiVP and is discussed in the next section. Glikson et al. also indicate that it may be appropriate to choose CSP over BiVP for CRT in the presence of specific patient populations in whom a simpler device is desired (older and frail patients in particular, who are frequently those referred for AVJA).43

Another indication of cardiac pacing is tachy–brady syndrome. Indeed, permanent pacing with single- or dual-chamber pacemaker associated or not with AVJA may also be considered in patients with symptomatic AF associated with sick sinus syndrome. Those patients are frequently challenging to manage, with alternating slow heart rate due to sinus node dysfunction and fast heart rate due to paroxysmal AF. This strategy is particularly interesting in cases of poorly tolerated antiarrhythmic drugs (worsening bradycardia) or unsuccessful/unfeasible AF ablation in frail and elderly patients.

Finally, AVJA can be indicated in patients with a previously implanted pacemaker when AF is rapidly conducted to ventricles. In patients with RVP for conduction disease (sinus node dysfunction or paroxysmal AV block), and cases of LV dysfunction, performing AVJA first can be discussed, then, following an evaluation of LVEF, upgrading the pacemaker to BiVP or CSP if there is persistent LV dysfunction.

In patients with CRT who cannot achieve permanent BiVP due to high-rate supraventricular tachycardia, AVJA can also be indicated. The effectiveness of CRT pacing is highly determined by the percentage of biventricular capture beats, which must be at least >90–95%, and as close to 100% as possible. Rapidly conducted AF frequently interferes with pacing, with an estimated two-thirds of patients with persistent or permanent AF who cannot reach this objective of biventricular capture.47 The small JAVA-CRT pilot trial (n=26) evaluated the role of AVJA in CRT-eligible patients with permanent AF and whether it could enhance CRT efficacy. Its limited sample size provided inconclusive results, with no significant differences in LV function or clinical outcomes between arms.48 More recently, the CAAN-AF trial (ESC 2025) investigated a similar clinical question in a larger randomised population (n=143) but was stopped early for futility.49,50 Despite neutral findings, the results suggest that patient heterogeneity and high baseline BiVP rates may dilute potential benefits, underscoring the need for adequately powered studies in appropriately selected patients.50 It is therefore recommended that symptomatic patients implanted with a CRT pacing device, experiencing permanent AF, New York Heart Association class III or IV and incomplete BiVP capture due to AF, should benefit from AVJA, in order to reduce mortality, HFH and relieve HF symptoms (class 2a, level of evidence b).44

As pace-and-ablate evolves, AF ablation has also seen major advances in recent years, notably with the advent of pulse field ablation (PFA). PFA has altered the balance between rhythm and rate control by combining noninferior efficacy, compared with thermal ablation techniques, with a favourable safety profile supporting a lower threshold for de novo or repeat ablation in older and higher-risk patients.

Despite these improvements in AF ablation and the subsequent changes in the decision-making process, AVJA can still be preferred as first-line therapy in the following situations: AF and a need to guarantee near-100% ventricular capture in patients already implanted with CRT; low expected rhythm-ablation success (extensive atrial remodelling, markedly enlarged left atrium [LA], infiltrative cardiomyopathies) where rate regularisation is the principal therapeutic goal; a contraindication to LA ablation (e.g. persistent LA thrombus) or urgent need to reverse tachycardia-mediated LV dysfunction; and patient preference for a single, definitive rate-control pathway after shared decision-making.

No randomised trial has directly compared repeat catheter ablation versus AVJA plus pacing as first- or subsequent-line therapy; therefore, decisions about redo AF ablation procedures should remain individualised and anchored in patient phenotype, comorbidities and goals of care.

Device Therapy Options: From Right Ventricular to Biventricular Pacing or Conduction System Pacing and From Transvenous to Leadless Pacemakers

Permanent pacing is mandatory once the AV junction has been ablated. Device choice now spans a broad spectrum, each option offering distinct electrophysiological benefits, implantation challenges and long-term prognostic implications. This section summarises the evidence base (Table 1 ) and provides a pragmatic framework (Table 2) for selecting the most appropriate system in patients with AF undergoing AVJA.

Table 1: Randomised Control Trials on Atrioventricular Junction Ablation for the Treatment of AF

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Table 2: Comparison of Pacing Options after Atrioventricular Junction Ablation for AF

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Right Ventricular Pacing

RVP remains the historical and most widely available solution. However, RVP is also known for its detrimental effects on ventricular contraction. Early observational registries and the DAVID, MOST and PACE randomised trials showed that chronic RVP may induce electrical and mechanical dyssynchrony, leading to pacing-induced cardiomyopathy in up to 20% of patients, particularly when the pacing burden is high and LVEF is already reduced.51–55 In addition, post-ablation cohorts confirm a lesser improvement in LVEF and higher HFH rates compared with BiVP or CSP modalities.56–59 RVP is therefore considered as acceptable in elderly, frail patients with preserved LVEF and narrow QRS complexes when implantation time and cost must be minimised and the expected lifespan is short. In all others – in particular those with pre-existing cardiomyopathy or a wide QRS – a more physiological pacing strategy is preferred.

Biventricular Pacing

BiVP prevents the electrical and mechanical dyssynchrony created by RVP and therefore improves outcomes. A randomised controlled trial and a meta-analysis confirmed the benefit of BiVP over RVP in patients undergoing AVJA.60,61 In addition, the APAF-CRT trials demonstrated that, in patients with AF with narrow QRS and HF who underwent AVJA, systematic BiVP reduced all-cause mortality by 74% versus pharmacological rate control.46,62 Hence, BiVP should be considered (class 2a) in combination with AVJA in severely symptomatic patients with permanent AF and at least one HFH to reduce symptoms, physical limitations, recurrent HFH and mortality.1

However, BiVP has some limitations resulting from the use of more complex devices and materials, leading to a significant rate of complications. First, the implantation requires extra skills in positioning the LV lead into the coronary sinus branches, especially in those with HF with enlarged LVs.63 In such cases, the LV leads have a particular propensity for complications such as dislodgement and coronary vein dissection or perforation and are more commonly associated with complications compared with RV leads (4.3% versus 2.2%).64,65 Significant diaphragmatic stimulation (up to 5% of procedures) and generator battery depletion are also concerns, exposing the patient to a higher hospitalisation rate for re-intervention.66,67 In a retrospective study comparing BiVP and RVP devices, 50% (versus 10%) of patients with BiVP devices underwent surgical revision for battery depletion in the 4 years of implantation, and 14% (versus 4%) for unanticipated events such as LV lead dislodgement or lead infection.68 Finally, by requiring more leads and specific material, BiVP procedures are longer with an increased risk of lead dislodgment or device infection, and at higher costs compared with RVP.64,65,69 For those multiple reasons, some operators can be reluctant to propose BiVP to every patient, particularly those who may be in frail and comorbid condition, even in this particular context of AVJA.

Conduction System Pacing

The introduction of permanent CSP in the form of HBP and left bundle branch area pacing (LBBAP) allows physiological pacing and is a serious alternative to RVP and BiVP.70

His-Bundle Pacing

Implanting the His-bundle lead first and proceeding to AVJA in the same session (implant-then-ablate) has become an appealing alternative to conventional RVP for rate-control-refractory AF. By recruiting the native His–Purkinje network, HBP maintains near-physiological ventricular activation and avoids the dyssynchrony-mediated decline in LVEF and excess HFH typical of chronic RVP.

Prospective and retrospective cohorts consistently show significant reverse remodelling: LVEF increases and end-systolic volumes fall within 6–18 months of the combined procedure.71–73 In the largest multicentre study to date (n=223), Vijayaraman et al. reported a 39% lower risk in the composite of death + HFH compared with RVP.72 HBP has been demonstrated in several small randomised trials and larger non-randomised studies to be superior to RVP and even at least as good as BiVP post-atrioventricular nodal ablation (AVNA).74,75 On the basis of these data, the 2025 ESC/European Heart Rhythm Association and 2023 HRS/APHRS/LAHRS guidelines awards HBP a class 2a recommendation for pace-and-ablate with rapid AF.42,43 However, its feasibility alongside AVNA must be considered in light of the unique challenges posed by the close proximity of the ablation site to the pacing electrode and the general concern about late rises in capture thresholds frequently necessitating an RV backup lead or high re-intervention rates (≈10–15%).76,77

Left Bundle Branch Area Pacing

The aim of LBBAP is to target the left side of the septum and capture the left bundle branch by penetrating the interventricular septum. Several cohort studies and meta-analyses have shown LBBAP to be superior to conventional pacing (RVP and BiVP) regarding LVEF improvement and mortality and HFH reduction from the first year.58,78 While LBBAP ensures physiological activation of the LV, it creates a right bundle branch block activation pattern leading to concerns about the lack of physiological activation of the RV. However, recent RV free wall strain assessment during echocardiographic evaluation has seen improvements in RV systolic function with LBBAP.79 Propensity score matching analysis of a pace-and-ablate strategy of LBBAP versus HBP patients reported similar improvements in echocardiographic and HF outcomes, whereas higher implant success rates, better pacing parameters and fewer late lead-related complications were present in the LBBAP group.80 Importantly, late increased thresholds were noted in 9.3% of the HBP group requiring reprogramming to RVP via the previously placed backup lead. These results were confirmed in a recent meta-analysis.78 Hence, LBBAP seems to be the preferred CSP option for pace and ablate strategy.81 In patients who have failed LBBAP, HBP may offer an excellent bailout pacing option.82

Leadless Pacing

Leadless pacing (LP) offers an attractive hardware-minimising alternative to transvenous systems for frail and anticoagulated patients such as those referred for pace and ablate strategy. The self-contained capsule delivered percutaneously via the femoral vein offers the advantage of abolishing the risks of pocket haematoma, lead fracture and minimising infection and tricuspid interference. LP also offers the possibility to proceed, with acceptable safety, to a concurrent AVNA without prolonging procedure time.83 One can expect in the near future the meeting of LP and CSP as recently described by Reddy et al.84 By combining the best of the two worlds, this solution may facilitate the decision-making process in favour of this pace-and-ablate strategy, especially in frail and elderly patients.

When to Add ICD Capability?

Few data are available in this specific population. Hence, ICD indications in patients requiring AVNA do not differ from patients not requiring AVNA, although a non-negligible proportion of these patients will have restored LVEF thanks to slowing down the heart rate and will no longer subsequently benefit from ICD capability. ICD is therefore indicated in patients with LVEF ≤35% for primary prevention or in case of secondary prevention whatever the mode of stimulation: BiVP-defibrillator and CSP-defibrillator or LP + subcutaneous defibrillator.44

Pacing Options Before Atrioventricular Junction Ablation: A Tailored Approach

The contemporary evidence supports a personalised approach regarding which LBBAP or HBP is preferred for most pacing-dependent HF patients: BiVP remains the standard when LVEF is reduced, leadless devices serve selected high-risk patients and RVP is reserved for cases of failed CSP or for low-risk or palliative scenarios (Figure 2). On-going trials, such as PACE-FIB (NCT05029570) comparing LBBAP plus AVNA versus pharmacological rate control in patients with permanent AF and HF with preserved or minimally reduced EF and ABACUS (NCT06207383) comparing AVNA plus CSP versus pulmonary vein isolation in patients with persistent AF and symptomatic HF aged >60 years, will give us new insights and levels of evidence.

Figure 2: Device Selection Flowchart for Pace-and-ablate Strategy

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Atrioventricular Junction Ablation Options

AVJA can be achieved by targeting the compact AV node within the triangle of Koch or – when needed – the His bundle; both create complete AV block, with the node-first approach generally preferred to preserve a backup escape rhythm in case of pacing threshold rise or lead dislodgment and to limit interaction with CSP leads.85 In a pace-and-ablate strategy, most operators implant the device first and then perform AVJA either in the same sitting or after a short interval to confirm lead stability – especially relevant for HBP, where radio frequency near the His may transiently raise capture thresholds. However, same-time AVJA can be performed especially after leadless pacemaker implantation using the same femoral venous access.83 Observational series indicate that AVJA after HBP is feasible with generally stable pacing parameters, while comparative data suggest that LBBAP interacts less with ablation (higher acute ablation success and fewer lead-related issues), likely owing to the greater spatial separation between the AV node ablation site and the LBBAP lead.58,86

Conclusion

AVJA offers a viable and often underused option for patients with AF and symptomatic or refractory HF, particularly when rate or rhythm control strategies fail. Evidence supports its benefit in reducing morbidity and improving functional status, especially when combined with BiVP or CSP to prevent pacing-induced dyssynchrony. Careful selection of both the patient and the pacing strategy is essential to optimise outcomes. As device technology and physiological pacing techniques evolve, the ablate-and-pace approach should be integrated into individualised treatment pathways for patients in whom sinus rhythm cannot be maintained or restored.

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