What is the incidence and electrophysiologic profile of inadvertent diaphragmatic or psoas muscle stimulation by leadless pacemakers after several hours of recumbency, and can postural change reliably terminate these extra‑cardiac stimulations?
True extra‑cardiac capture by a leadless pacemaker is very uncommon (< 1 % of implants), tends to appear only after hours of recumbency when the device or the heart has shifted just enough to let the stimulus reach the phrenic/diaphragmatic or iliopsoas nerves, and it almost always stops the moment the patient sits or stands.
| Device / Study | N (patients) | Extra‑cardiac stimulations reported | Incidence |
|---|---|---|---|
| Aveir DR dual‑chamber first‑in‑human cohort | 381 | 3 episodes in 2 patients | 0.5 % |
| Aveir VR single‑chamber (Leadless II pivotal, Phase 2) | 196 | 0 adjudicated extra‑cardiac captures at 6 weeks; event listed as potential AE only | < 0.5 % (upper 95 % CI ≈ 1.9 %) |
| Micra global investigational & post‑approval registries (≈ 2 700 implants combined) | — | Sporadic case reports only (no signal in pre‑specified SAE tables) | ≪ 1 % – exact numerator suppressed but classified as “rare” |
| Published single‑case literature (Micra, Aveir, Nanostim) | ≥ 10 cases (2017‑2025) | Hiccups, abdominal “thumping”, psoas jerks | Qualitative evidence |
Bottom line: Across the largest data sets the cumulative risk settles in the 0.1 – 0.6 % range, consistent with manufacturer information that still lists phrenic/diaphragmatic or “extra‑cardiac” capture as a potential—but very rare—adverse event.
| Parameter | Typical finding when extra‑cardiac capture is present | Mechanistic note |
|---|---|---|
| Output at which capture occurs | ≥ 2–5 V @ 0.24–1 ms (often near the safety margin used overnight) | High‑output back‑up pacing or rising thresholds after micro‑dislodgement put the stimulus above phrenic/psoas motor threshold. |
| ECG / EGMs | Normal ventricular capture, but an extra surface spike may coincide with abdominal wall contraction; myocardial thresholds often simultaneously elevated. | Confirms that both the ventricle and the nerve are being stimulated. |
| Vector dependence | Specific device–myocardium orientation (“septal nose‑up”) reproduces the phenomenon; altering the cathode/anode vector during manual pacing often turns it on/off. | Five separate Micra vectors reproduced diaphragmatic capture in a paediatric case. |
| Time / posture | Appears after several hours supine; disappears immediately on sitting or standing. | Supine position raises the diaphragm and shortens the distance between the RV apex/septum and the phrenic nerve; gravity reverses it. |
Together these effects often terminate capture within seconds—hence the “I get up and it stops” description many patients give.
True iliopsoas stimulation is even rarer than phrenic capture; only isolated conference abstracts and manufacturer adverse‑event reports describe hip‑flexor jerks or groin fasciculations linked to a leadless device, usually when the pacemaker lies unusually low in the RV outflow tract or has micro‑perforated toward the septal wall of the diaphragm. In every publicised instance, repositioning or explant solved the problem and posture had the same “on/off” effect.
In summary: Extra‑cardiac stimulation from leadless pacemakers is a very low‑incidence event, characterised by high‑output, posture‑dependent diaphragmatic or (rarely) psoas capture that is instantly relieved by standing. When it does occur, simple re‑programming or redeployment of the capsule almost always cures the problem, but systematic prospective data are still scarce.