From Aveir VR to LBBAP: Anatomy of an Early PICM Upgrade Decision

A first-person case report on recognizing early pacing-induced cardiomyopathy in a leadless pacemaker recipient and the intraprocedural criteria that defined a successful conduction system pacing upgrade.

📅 Published April 23, 2026 🫀 Electrophysiology ⏱️ 12 min read

Early pacing-induced cardiomyopathy rarely announces itself with a dramatic drop in ejection fraction. More often it speaks in a quieter vocabulary — eccentric remodeling at preserved EF, a drifting hs-TnT, a left atrium that expands without an obvious explanation. This is a case report about listening to that vocabulary early, and about the intraprocedural criteria that distinguish a credible LBBAP from a septal lead that merely looks the part.

Disclosure: This article is a first-person case narrative written from the perspective of the physician-patient. All data has been reviewed and anonymized for publication. Clinical findings are reported to advance physician education on early PICM recognition and LBBAP upgrade criteria. Dr. Sharma gave permission to be named as the implanting electrophysiologist.

The Index Device and the Reason for Concern

The patient — a male in his seventh decade, active competitive athlete, physician — received a single-chamber Abbott Aveir VR leadless pacemaker approximately two years prior to the upgrade described here. The original indication was intermittent high-grade AV block. At implant, pacing parameters were excellent and the clinical rationale for a leadless platform was sound: minimize pocket-related complications, preserve upper extremity venous anatomy, and accept the trade-off of right ventricular apical/septal pacing in a patient expected to have a low ventricular pacing burden.

The pacing burden, as it turned out, drifted upward. By the second year, ventricular pacing exceeded 90%. What followed is the story most electrophysiologists will recognize.

The soft signals

Serial echocardiography showed a constellation of changes at preserved left ventricular ejection fraction (~55%):

In parallel, high-sensitivity troponin T (hs-TnT) was chronically elevated above the 99th percentile reference, without an alternative ischemic explanation and with unremarkable coronary anatomy. Taken in isolation, any one of these findings could be dismissed. Taken together, they outlined the early phase of pacing-induced cardiomyopathy — the phase before EF falls, when the window for reversal is widest.

Clinical reasoning
The traditional PICM definition — a ≥10% drop in EF to below 50% — captures late disease. A growing body of evidence supports earlier recognition using remodeling, atrial volumes, strain imaging, and troponin kinetics. Waiting for the EF to fall is, in many patients, waiting too long.

Why LBBAP, and Why Now

Three converging arguments drove the decision to upgrade rather than continue surveillance:

  1. Electrical substrate. A paced QRS of 212 ms represents roughly 100 ms of avoidable activation delay versus native or conduction-system-paced morphology. That delay is the mechanical dyssynchrony that drives the remodeling.
  2. Biomarker evidence. Chronically elevated hs-TnT in a non-ischemic patient with high RV pacing burden is, in the framework proposed by several PICM investigators, a signal of ongoing subclinical myocardial strain.
  3. Morphologic trajectory. The eccentric remodeling and LA dilation were progressive on serial studies — not a single outlier echo but a trend.

The choice of LBBAP over biventricular pacing was driven by the physiology of the substrate. This was not classic CRT-indication HFrEF with left bundle branch block; this was iatrogenic dyssynchrony from RV pacing in a previously narrow-QRS heart. Conduction system pacing recruits the native His-Purkinje network and restores near-physiologic activation — theoretically superior, and increasingly supported by LBBP-RESYNC, HOT-CRT, and other trials, to biventricular pacing in this specific scenario.

The Procedure: What "Non-Selective LBB Capture" Actually Looks Like

The upgrade was performed by Dr. Parikshit Sharma at Cleveland Clinic Florida (Weston). The Aveir VR was explanted via snare retrieval — feasible and uncomplicated at the two-year timepoint — and replaced with a transvenous dual-chamber system: a Medtronic 5076-45 atrial lead to the right atrial appendage, and a Medtronic 3830 lumenless lead delivered via C315 sheath to the left bundle branch area.

Mapping and targeting

After mapping the His bundle region, a site approximately 1–2 cm distal was selected for LBB lead deployment — the standard Huang-technique landing zone on the left ventricular side of the interventricular septum. The lead was advanced by rotational deployment while pacing parameters and paced QRS morphology were monitored continuously.

The criteria that defined capture

This is the section that matters most for physicians considering or performing LBBAP. A lead deep in the septum is not automatically a conduction-system-capturing lead. Four independent criteria were documented intraprocedurally:

Table 1. Intraprocedural LBBAP capture criteria
CriterionObservedInterpretation
LVAT (V6 R-wave peak time)67 ms, fixedBelow 75 ms threshold; fixed across outputs = conduction capture, not myocardial-only
V6–V1 interval70 msConsistent with left bundle rather than left septal myocardial capture
NS → S-LBBP transitionDemonstratedGold-standard criterion; only possible with true bundle engagement
Paced morphologyrsR' in V1; S waves in I and V6Expected RBBB-pattern of LBBAP
The "fixed LVAT" point is critical
Many septal leads produce an acceptable-looking paced QRS. What distinguishes true conduction system capture is that the V6 R-wave peak time does not change when the pacing output is increased or decreased — the wavefront is propagating through the specialized conduction system at its intrinsic velocity, not through myocardium whose activation speed varies with capture strength. A shifting LVAT with output is the signature of left septal pacing masquerading as LBBAP.

Electrical reconfiguration

The immediate electrical result was striking:

That 100 ms is not cosmetic. It is the electrical substrate on which reverse remodeling, if it occurs, will be built.

Implant Parameters and What They Tell Us

Table 2. Implant pacing parameters
ParameterLBB lead (RV position)Atrial lead
Capture threshold1.00 V @ 0.4 ms1.25 V @ 0.4 ms
R/P-wave amplitude4.3 mV bipolar / 8.7 mV unipolar1.8 mV
Lead impedance703 Ω bipolar / 665 Ω unipolar437 Ω
Diaphragmatic stim at max outputNoneNone

A few observations on these numbers, because the quality of an LBBAP implant is as much about impedance and sensing reserve as it is about the paced morphology:

Atrial lead watch-point
The atrial P-wave amplitude of 1.8 mV is acceptable at implant but on the modest side. Worth flagging at the first in-office interrogation; atrial sensing drift is more common than ventricular sensing drift, and low atrial sensing is a recognized source of mode-switching artifacts.

What We Expect to See Over the Next Twelve Months

The hypothesis — that the soft signals of early PICM were driven by RV pacing and will regress with conduction system pacing — is falsifiable. That is its scientific virtue and also its clinical utility. A prespecified surveillance plan looks like this:

Short term (0–3 months)

Intermediate (3–6 months)

Long term (12 months)

What would falsify the hypothesis
If at 6–12 months the LV dimensions continue to grow, hs-TnT remains elevated, and LA volume continues to expand, then RV pacing was not the sole driver of remodeling and an alternative cardiomyopathic process must be entertained. Prespecifying this endpoint is what separates a clinical decision from a clinical hope.

Takeaways for the Practicing Electrophysiologist

  1. PICM recognition should precede EF decline. Eccentric remodeling, LA dilation, diastolic dysfunction, and chronically elevated hs-TnT in a high-RV-pacing-burden patient are actionable signals — even with preserved EF.
  2. Leadless single-chamber devices are not PICM-proof. The pacing burden at two years is often higher than predicted at implant, and RV pacing is RV pacing regardless of delivery platform.
  3. LBBAP criteria must be met rigorously. A deep septal lead with acceptable thresholds is not an LBBAP implant. Fixed LVAT, V6–V1 interval, and NS→S-LBBP transition are the language of real conduction system capture.
  4. A 100 ms QRS narrowing is a prognostic number. The magnitude of electrical resynchronization at implant correlates with the probability of mechanical reverse remodeling.
  5. Pre-specify the surveillance endpoint. A hypothesis that cannot fail is not a hypothesis.
Medical disclaimer: This case report is intended for physician education and does not constitute medical advice for any individual patient. Clinical decisions must be individualized by the treating electrophysiologist based on full patient context. The authors have no financial relationships with Abbott or Medtronic to disclose relevant to this report.

Selected References

  1. Huang W, Su L, Wu S, et al. A novel pacing strategy with low and stable output: pacing the left bundle branch immediately beyond the conduction block. Can J Cardiol. 2017;33(12):1736.e1-1736.e3.
  2. Jastrzębski M, Kiełbasa G, Cano O, et al. Left bundle branch area pacing outcomes: the multicentre European MELOS study. Eur Heart J. 2022;43(40):4161-4173.
  3. Vijayaraman P, Ponnusamy S, Cano Ó, et al. Left bundle branch area pacing for cardiac resynchronization therapy: results from the International LBBAP Collaborative Study Group. JACC Clin Electrophysiol. 2021;7(2):135-147.
  4. Wang Y, Zhu H, Hou X, et al. Randomized trial of left bundle branch vs biventricular pacing for cardiac resynchronization therapy (LBBP-RESYNC). J Am Coll Cardiol. 2022;80(13):1205-1216.
  5. Kiehl EL, Makki T, Kumar R, et al. Incidence and predictors of right ventricular pacing-induced cardiomyopathy in patients with complete atrioventricular block and preserved LVEF. Heart Rhythm. 2016;13(12):2272-2278.
  6. Khurshid S, Epstein AE, Verdino RJ, et al. Incidence and predictors of right ventricular pacing-induced cardiomyopathy. Heart Rhythm. 2014;11(9):1619-1625.