ABC FARMA
Clinical Cardiology & Electrophysiology Reference

LBBAP After Aveir VR Leadless Pacemaker: When AV Synchrony Cannot Be Achieved and Whether to Plan for an Aveir DR Upgrade

Published: April 30, 2026 | Cardiac Electrophysiology | Pacing & Devices | Reading time: ~10 min
Summary: A 71-year-old male with lifelong sinus bradycardia (~48 bpm), six years of atrial flutter, prior atrial flutter ablation, and two years of single-chamber Aveir VR leadless ventricular pacing underwent upgrade to left bundle branch area pacing (LBBAP). During the procedure, the operator increased the paced rate from 50 to 60 bpm in an attempt to unmask sinus P-wave activity for atrial sensing assessment, but no usable atrial signal emerged. This article analyzes why intra-operative atrial unmasking failed in this clinical phenotype, explains why this finding does not represent failure of LBBAP, and addresses the question of whether to plan for a future Aveir DR dual-chamber leadless pacemaker upgrade.

Clinical Background

Case profile: 71-year-old male, competitive rower, with the following longitudinal cardiac history:
  • ~50 years of constitutional sinus bradycardia at approximately 48 bpm (lifelong baseline)
  • 6 years of atrial flutter
  • Atrial flutter ablation (~4 years ago)
  • 2 years of single-chamber Aveir VR leadless RV pacing for complete heart block
  • Documented progressive LV ejection fraction decline (from ~56% to 45–55% range)
  • Persistently elevated high-sensitivity troponin T (~40–42 ng/L)
  • ~97% RV pacing burden on most recent device interrogation
  • Capture threshold rise from 2.75 V to 3.5 V on the most recent check
  • Recent LBBAP upgrade procedure

Intra-Operative Strategy and Outcome

The operating electrophysiologist had planned to program a lower rate of 50 bpm — matching the patient's chronic baseline. During the procedure, an attempt was made to raise the paced rate to 60 bpm in order to bring the lower rate above the patient's intrinsic sinus rate. The therapeutic question this maneuver was designed to answer: can the patient's atrium produce a sensable, organized P wave that could later support an atrial-sensing or atrial-pacing device?

Despite the rate adjustment, no clear sinus P wave emerged on the recording. Post-procedural single-lead and 6-lead ambulatory ECG tracings continue to show paced QRS complexes at 60 bpm with no antecedent P wave in any limb lead — consistent with either functional overdrive suppression of a slow sinus node, advanced sinus node dysfunction with atrial myopathy, or atrial standstill.

Why the Atrium Did Not Cooperate: Differential Diagnosis

The key conceptual point: P-wave "recovery" at a higher paced rate is not something the operator creates — it is something the patient's sinus node and AV conduction either permit or do not. Raising the lower rate is a probe, not an intervention. In this patient, the probe returned a discouraging answer for several converging reasons.

1. Procedural sedation suppressing an already-slow sinus node

Procedural sedation agents (midazolam, fentanyl, propofol) blunt sympathetic tone and lower the intrinsic sinus rate. In a patient whose lifelong baseline rate is already 48 bpm, sedation can drop it further — into the low 40s or below. If the device paces at 60 while the sinus node is firing at 45, every cycle is captured by the pacemaker before the sinus node can fire (functional overdrive suppression), and no P waves will appear on the surface ECG. This is the most common transient cause of intra-operative failure to unmask atrial activity.

2. Binodal disease (concurrent sinus node dysfunction)

The fibrotic and degenerative processes that produce complete AV block frequently affect the sinus node as well. A patient with a 50-year history of bradycardia at 48 bpm, who later developed flutter and then complete heart block, very likely has structural disease at both nodes. In this setting, an intrinsic sinus rate consistently below the device's lower rate is the rule, not the exception. Ambulatory Kardia trends in this case showing a steady 50 bpm — exactly matching the device lower rate — confirm that the sinus node essentially never beats the pacemaker.

3. Post-flutter atrial myopathy

Six years of atrial flutter, followed by ablation lines, followed by two years of pacing without AV synchrony, produces measurable structural and electrical remodeling of the atrium: dilation, fibrosis, loss of contractile reserve, and reduction in usable myocardial substrate. In some patients this progresses toward atrial standstill — a clinical state in which there is no organized P-wave activity at any rate, with or without pharmacologic provocation.

4. Retrograde ventriculoatrial conduction

With LBBAP, retrograde conduction up the His–Purkinje system to the atrium is possible. If each paced ventricular beat conducts retrograde and resets the sinus node, the sinus node never has time to fire spontaneously — the atrium is captured retrogradely on every cycle. This is testable with formal VA conduction assessment during the implant.

5. Subclinical atrial fibrillation

Catheter manipulation in the right atrium during an LBBAP implant can provoke transient AF, particularly in a patient with prior atrial flutter and remodeling. Fibrillatory activity at low amplitude on a 6-lead recording may not be obvious without higher gain or a longer rhythm strip.

Clinical pearl: The intra-operative attempt to find a P wave at a higher paced rate is a feasibility test for atrial sensing — not a treatment. A negative result is informative: it shapes whether a future dual-chamber strategy (transvenous or leadless) is worth pursuing, and whether AV synchrony is recoverable at all in this patient.

Has LBBAP "Failed"? A Reframe

It is tempting, after a discouraging intra-operative finding, to conclude that the entire LBBAP procedure has failed. This framing is incorrect.

LBBAP is designed to deliver physiologic ventricular activation via the conduction system, with the goal of preventing or reversing pacing-induced cardiomyopathy (PICM). In this patient, the ventricular problem — chronic 97% RV pacing burden, progressive EF decline, elevated troponin — is precisely what LBBAP addresses, and it does so well. The procedure achieved its primary goal: replacement of non-physiologic apical RV pacing with conduction-system pacing.

What was not achieved is AV synchrony — and AV synchrony was never going to come from an LBBAP lead alone. AV synchrony requires either an atrial lead, an atrial-sensing algorithm, or a separate atrial pacing device. The intra-operative maneuver to find a P wave was a diagnostic probe to see whether any atrial-based strategy would be feasible in this patient. The answer it returned: probably not, at least not under the conditions tested.

The accurate framing: LBBAP succeeded at fixing the ventricle. The atrium is the unsolved problem — and it may not be solvable at all.

The Aveir DR Question

A natural next question, particularly in a patient who already has an Aveir VR leadless pacemaker, is whether to plan for an upgrade to the Aveir DR (dual-chamber leadless) system in the future. The Aveir DR is the first dual-chamber leadless pacemaker system and provides true atrial and ventricular pacing with wireless inter-device communication for AV synchrony. Implant success rates in pivotal studies are high (~99%).

However, this patient's situation introduces several specific complications that the standard "Aveir VR → Aveir DR" upgrade pathway does not address.

The hardware reality after LBBAP

After LBBAP upgrade, this patient is no longer running a leadless-only system. He has:

  1. An Aveir VR leadless pacemaker in the right ventricle
  2. A new transvenous LBBAP lead and pulse generator

The clean Aveir VR → Aveir DR upgrade pathway that Abbott markets is for patients whose only hardware is a single Aveir VR. This patient is past that exit point.

The atrial substrate is the rate-limiting factor — not the hardware

Adding an Aveir AR (atrial leadless) or any dual-chamber system requires a sensable, captureable atrium with reasonable conduction properties. Given this patient's history — six years of flutter, ablation, deconditioning, lifelong slow sinus, and now a failed intra-operative atrial unmasking probe — there is a real possibility that no atrial pacing device will give this patient meaningful AV synchrony, leadless or transvenous. The labeled indication for atrial-only or dual-chamber leadless pacing assumes a working atrium. This patient's phenotype does not fit that population.

Hardware abandonment and extraction risk

If the patient pursues a leadless dual-chamber strategy in two years, the question of what to do with the existing LBBAP lead and pulse generator becomes non-trivial. Options include leaving the lead capped (with chronic indwelling lead risks: infection, venous occlusion), extracting the lead (a procedure that is not trivial in a 73-year-old with a 2-year-old fixation lead), or attempting some hybrid configuration. None of these are clean.

The simpler upgrade — if AV synchrony is recoverable

If reassessment in 6–12 months suggests that the atrium is in fact pacable and sensable, the standard-of-care upgrade pathway is adding a transvenous atrial lead to the existing LBBAP system. The pocket and generator are already in place. This converts a single-chamber LBBAP system into a dual-chamber DDD LBBAP — true conduction-system pacing with full AV synchrony — and is technically straightforward. This pathway has the same atrial-substrate prerequisite as a leadless dual-chamber strategy, but it is mechanically simpler, lower risk, and does not require abandoning recently implanted hardware.

A Recommended Decision Sequence

Step 1 — Characterize the atrium (now to 6 months): 14- to 30-day ambulatory monitoring at current device settings. Echocardiogram with strain imaging to assess atrial size, function, and remodeling. Question to answer: does this patient have a viable atrium?

Step 2 — Reassess ventricular response to LBBAP (6–12 months): Repeat echocardiography for EF recovery, hs-TnT trend, and BNP/NT-proBNP. If LBBAP is doing its job — EF recovers, troponin normalizes, functional capacity improves — the urgency of restoring AV synchrony drops considerably. Many patients with chronic atrial disease do well on optimized rate-responsive ventricular conduction-system pacing.

Step 3 — Hardware decision (only if Steps 1–2 indicate a viable atrium AND symptomatic benefit from AV synchrony is the limiting factor): The conversation at that point is between adding a transvenous atrial lead to the current system versus abandoning the system to go all-leadless. In a patient who already has a working transvenous LBBAP system, the transvenous atrial lead addition is almost always the simpler, safer, lower-risk option.

Bottom Line

The two-year planning question should not be "which device next?" The two-year planning question should be: "Is this atrium worth pacing at all?"

This is the question that drives the decision. Hardware choices follow from the answer — they do not precede it.

Medical disclaimer: This article is intended for healthcare professionals and informed patients as a clinical reference. It is not a substitute for individualized medical advice from a qualified cardiac electrophysiologist who has direct access to the patient's full clinical record, device interrogation data, and imaging studies. Device selection, programming, and upgrade strategies must be individualized.
Selected references:
  1. Knops RE, et al. A Dual-Chamber Leadless Pacemaker. N Engl J Med 2023; DOI: 10.1056/NEJMoa2300080.
  2. Reddy VY, Exner D, et al. 1-Year Outcomes of a Leadless Ventricular Pacemaker: The LEADLESS II (Phase 2) Trial. JACC Clin Electrophysiol 2023.
  3. Aveir DR i2i Study (NCT05252702): Procedural outcomes of de novo dual-chamber leadless pacemaker implantation. Heart Rhythm 2025.
  4. Doshi RN, Ip JE, et al. Outcomes of patients implanted with an atrioventricular synchronous leadless ventricular pacemaker in the Medicare population. Heart Rhythm 2024;21:66–73.
  5. Vijayaraman P, et al. His–Purkinje Conduction System Pacing: State of the Art. JACC Clin Electrophysiol 2023.
  6. Merchant FM, et al. Pacing-Induced Cardiomyopathy: Mechanisms, Recognition, and Management. Circulation 2022.