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User question:
Pacemaker Output Voltage Increase and Ventricular Fibrosis
Pacemaker Output Voltage Increase and Ventricular Fibrosis
🔬 Is an increase in pacemaker output voltage (e.g., from 2.5V to 3.5V) an indication of fibrosis in the ventricle?
Possibly — yes, but not definitively. An increased pacing threshold (i.e., needing more voltage to achieve capture) can be associated with local fibrosis, inflammation, micro-dislodgement, or electrode encapsulation at the electrode-tissue interface.
✅ Why fibrosis could be involved:
Endocardial fibrosis around the cathode of a leadless pacemaker (like Aveir VR) may:
Increase tissue resistance
Disrupt the normal conductive interface
Require higher voltage to achieve reliable myocardial capture
This fibrotic process can develop over months after implantation, especially at areas of micro-motion or chronic low-grade inflammation.
⚠️ But other causes are possible too:
Tissue remodeling or scarring — especially if there has been prior ischemia, infarction, or cardiac disease.
Lead micro-dislodgement or suboptimal initial placement — can reduce tissue contact quality over time.
Battery conservation strategies at the time of implantation may have initially used the lowest acceptable voltage, and subsequent adjustments reflect safety margins being widened.
Autonomic or circadian variations — may alter capture thresholds, especially at night (e.g., during bradycardia).
Electrode-tissue interface changes — sometimes reversible, such as temporary inflammation or edema.
🔍 Diagnostic Clues:
If the threshold increased gradually over time, fibrosis is more likely.
If the threshold increased suddenly, it could be due to dislodgement or acute tissue changes.
An ECG with loss of capture or pacing artifacts not followed by QRS complexes would confirm the clinical need for higher voltage.
📌 Summary:
Yes, fibrosis is one plausible explanation for rising pacing thresholds, but it's not the only one.
Only imaging (like MRI if device-safe), device interrogation trends, or electrophysiologic mapping could confirm fibrosis.
Most commonly, clinicians opt to raise output to ensure capture rather than investigate the underlying pathology in leadless pacemakers—unless thresholds become unstable or battery life is at risk.