Does transient loss-of-capture at relatively high output (≥3 V @ 0.4 ms) indicate progressive fibrosis or electrode–myocardium interface inflammation, and can real-time Perfusion Index monitoring serve as a surrogate marker for impending threshold rise in leadless pacemakers?
| Clue in the device log | Pathophysiological reading | Supporting evidence |
|---|---|---|
| Stable R-wave sensing yet rising capture threshold and/or impedance | Thickened fibrotic sheath or thrombo-inflammatory tissue increases cathode–myocardium distance | [1], [2] |
| Sudden step-up in threshold that later normalises | Micro-edema, clot or partial dislodgement | [3] |
| Progressive threshold rise over months | Chronic fibrotic scarring, possibly systemic disease-linked | [4] |
| Rare long-term signal (~0.6%/year) | Recognized late complication in registry data | [5] |
Conclusion: A single failure at ≥3 V doesn't prove fibrosis, but it raises concern about biological degradation at the electrode interface. Monitoring trends (threshold, impedance, R-wave) and imaging are key for diagnosis.
| Rationale | Supporting insights |
|---|---|
| PI tracks stroke volume & vasomotor tone | [6] |
| Missed beats → ↓ SV → PI drops within 2–3 s | PI dips precede SpO₂ changes in pause-related bradyarrhythmias |
| Consumer wearables support cloud analytics | PI affected by temperature, tone, and probe location |