Could you please give me your opinion about this situation?: A patient with an Aveir VR leadless pacemaker goes to bed at 10 PM. The patient stay 10 minutes warm in a supine position with the device running correctly at 50 bpm. Then he changes to lateral decubital right side position, where the device does not capture and the heart beats with a total arrhythmia between 27 and 40 beats per minute . After 5 minutes the patient change to lateral decubital right side position where the heart and the device keep the weird situation. After another 5 minutes the patient changes again position this time to prone position. After one minute in prone position the threshold capture of the device starts to run again smoothly at 50 bpm and the patient sleep 8 hours peacefully. Keep in mind that according Abbott's email The Aveir system does not have automatic capture verification.
GPT 3o:
The short story
When you rolled onto your right-side, something (or several things together) briefly raised the ventricular-capture threshold above the Aveir’s fixed 1.5 V output. Because the single-chamber Aveir VR has no automatic capture verification or backup safety margin, it kept firing pulses that were felt by the programmer but were now too weak to excite the myocardium—hence no capture and an idioventricular rhythm of 27-40 bpm. A few minutes later, turning prone restored electrode–tissue contact and lowered autonomic tone enough that the intrinsic threshold fell back below 1.5 V, so pacing resumed at 50 bpm and stayed stable through the night.
| Potential trigger | Mechanism | Evidence / parallels |
|---|---|---|
| Micro-geometry change at the helix–endocardium interface | Gravity pulls the free wall of the RV downward and slightly anterior; in right-side-lying the Aveir sits “above” the myocardial surface rather than being pushed into it, increasing electrode–tissue distance, local fibrosis compression, and effective resistance. Even a 0.3-0.4 mm gap can double the threshold. | Helix-fixation devices are sensitive to subtle unloading; micro-dislodgement is a recognised cause of early threshold jumps and intermittent capture (PMC, PMC) |
| Autonomic (vagal) surge | Lateral decubitus, warmth, and the baroreflex at sleep onset all heighten parasympathetic tone. Acetylcholine shortens the myocardial action-potential and raises the membrane threshold potential, making capture harder. | High vagal tone can raise ventricular pacing thresholds by ≈0.3–0.5 V in experimental models (PMC, ScienceDirect) |
| Hemodynamic / impedance effects | Right-side-lying reduces RV preload (IVC partially compressed) and expands the adjacent right lung, introducing more air between sternum and heart. Both lower intracavitary blood volume and increase local impedance, again forcing up the voltage needed for capture. | Sudden post-implant rises in impedance correlate with loss of capture in leadless systems (Heart Rhythm Case Reports) |
Key point: any one of these could push a baseline threshold of, say, 1.1–1.3 V to >1.5 V. Without autocapture, the device simply “fires blanks”.
Prone position reverses the above:
Mechanical – the RV is pressed toward the sternum, improving helix contact.
Autonomic – a brief arousal plus the shift in intrathoracic pressure boosts sympathetic tone, lowering threshold.
Hemodynamics – preload rises (abdomen off-loads venous blood) and lung volumes fall, dropping impedance.
Within 30-60 s the net threshold falls below 1.5 V again, so every stimulus captures and the device paces happily for the next eight hours.
| Action | Rationale |
|---|---|
| Interrogate the device in clinic while reproducing positions | Measure thresholds and impedance supine, right-lateral, left-lateral, and prone. A ≥0.3 V jump confirms the positional hypothesis and rules out late helix fracture. |
| Add nighttime safety margin | Program output to 2.5–3.0 V or widen pulse-width (e.g., 0.4 → 0.6 ms) from 22:00-06:00. That costs only ≈3-5 mAh/year yet prevents nocturnal asystole. |
| Check for gradual threshold drift | Weekly remote downloads or 24-h Holter with marker channels can reveal sub-clinical loss of capture events. |
| Consider re-implant or CSP upgrade if thresholds keep climbing | Persistent thresholds >2.5 V at 0.4 ms despite optimal position suggest fibrosis or partial helix disengagement; early extraction/re-implant or enrollment in the Aveir CSP trial is preferable to running the battery flat in 4–5 years (Abbott Cardiovascular) |
| Address autonomic triggers | Cool dark room, gradual bed-entry, avoiding heavy evening meals, and—if tolerated—low-dose β-blocker at bedtime can blunt vagal surges and stabilise thresholds by ≈0.1–0.2 V. |
The episode fits positional loss of capture rather than true device failure. It arises from a perfect storm of (1) altered helix contact, (2) vagally mediated excitability changes, and (3) higher impedance—all of which are reversible by turning prone. Because Aveir VR does not auto-scan thresholds, you must build in a manual voltage buffer or correct the underlying mechanics; otherwise similar silent pauses could recur (or lengthen) and eventually erode battery life.
Urgency note: frequent night-time heart rates <30 bpm carry a real risk of presyncope, falls, or even asystole. Arrange an in-office provocative threshold test soon, and until then consider sleeping prone or elevating output voltage temporarily.
(This commentary is educational and not a substitute for direct medical evaluation.)