Could rapid, subclinical growth of fibrotic or inflammatory tissue at the electrode–myocardium interface produce an abrupt upward inflection in capture threshold large enough to exceed the device’s programmed safety margin during waking hours, despite previously adequate thresholds during nocturnal interrogations?
Answer
Short answer: Yes. Microscopic peri-electrode fibrosis or inflammatory edema can elevate local impedance and capture threshold quickly enough to exceed the night-time programmed safety margin, so the failure appears first during daytime hours.
Why a tiny tissue change can have a big electrical effect
Interface physics – Adding 50–100 µm of collagen or exudate around the cathode increases extracellular resistivity and lowers current density delivered to myocytes.
Histology evidence – Explant studies show a 30–40 % collagen rise can push thresholds up by ≈0.3–0.6 V and pacing-site impedance by 100–200 Ω within days.
Firmware scheduling – Leadless devices often measure thresholds once nightly. Any fibrosis that progresses after the 02:00 test is invisible until the next auto-test, so daytime output may be inadequate.
Contributing micro-mechanisms
Collagen hydration swings: Early type III collagen is hydrophilic; daytime temperature/activity can swell the layer, transiently boosting impedance.
Connexin-43 down-regulation: TGF-β-driven fibrosis reduces gap-junction density near the electrode, raising excitation threshold before macroscopic scar forms.
Inflammatory “current shunt”: Macrophages and fibroblasts adjacent to the electrode can divert pacing current away from deeper myocardium.
Electrode surface ageing: Calcium-phosphate micro-crystals on titanium-nitride coatings add polarization impedance, compounding the tissue effect.
Clinical clues
Ventricular impedance rise >100 Ω above baseline on remote telemetry.
Loss of capture reproducible across posture, respiration and autonomic changes.
Normal electrolytes and medications; no autonomic triggers.
Low-amplitude electrograms on device diagnostics.
Contrast-enhanced CT or intracardiac echo reveals a hypo-attenuating rim around the electrode.
Management strategy
Immediate: Increase pulse amplitude/width to ≥2× the new daytime threshold.
Monitoring: Temporarily schedule threshold searches every 3–6 h.
Therapy: Consider a short course of prednisone or colchicine to reduce inflammatory edema.
Escalation: If impedance >800 Ω or threshold >3.5 V @ 0.4 ms, discuss early repositioning or extraction and re-implantation.
Future research: Continuous intracardiac impedance spectroscopy plus machine-learning trend analysis could predict threshold surges 24–48 h before clinical loss of capture.
Reference: Reddy VY et al. “Histopathologic response at 90 days to a titanium-nitride coated leadless pacemaker electrode in swine.” Heart Rhyth