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Subsidiary pacemaker function in complete heart block after His-bundle ablation.

H Schmidinger1, P Probst, B Schneider

  • 1Department of Cardiology, University of Vienna, Austria.

Circulation
|October 1, 1988
PubMed
Summary
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His-bundle ablation can suppress ventricular impulse formation, leading to potential risks like Stokes-Adams attacks in patients with pacemakers. This study highlights rate-dependent overdrive suppression in subsidiary ventricular pacemaker tissue.

Area of Science:

  • Electrophysiology
  • Cardiology
  • Pacemaker Technology

Background:

  • His-bundle ablation is a treatment for certain heart conditions.
  • Understanding ventricular impulse formation post-ablation is crucial for patient management.
  • Subsidiary pacemaker function can be affected by external stimulation.

Purpose of the Study:

  • To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation.
  • To assess the impact of incremental ventricular overdrive stimulation on pacemaker function.
  • To determine the clinical significance of these findings in patients with pacemakers.

Main Methods:

  • Performed incremental ventricular overdrive stimulation studies in 11 patients post-His-bundle ablation.

Related Experiment Videos

  • Utilized both invasive temporary leads and noninvasive implanted pacemakers for stimulation.
  • Increased pacing rate incrementally, with a 2-minute duration at each level.

    • Main Results:

    • Ten of 11 patients exhibited a reliable ventricular escape rhythm.
    • 83% of studies showed progressive suppression of ventricular impulse formation with increased pacing rates.
    • Ventricular recovery time and post-recovery subsidiary pacemaker function were affected by overdrive stimulation.

    Conclusions:

    • Demonstrated rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue.
    • Findings are clinically important for patients with complete heart block and rate-adaptive pacemakers.
    • Sudden pacemaker inhibition at high rates may precipitate Stokes-Adams attacks.