Why the study?
Does incremental ventricular overdrive stimulation cause rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue in patients with complete heart block after His-bundle ablation?
Does incremental ventricular overdrive stimulation cause rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue in patients with complete heart block after His-bundle ablation?
Incremental ventricular overdrive stimulation causes rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue, highlighting a risk of Stokes-Adams attacks if rate-adaptive pacemakers fail at high rates.
May signal Stokes-Adams risk if rate-adaptive pacemakers fail at high rates; hypothesis-generating in post-ablation complete heart block.
To investigate the electrophysiological properties of ventricular impulse formation after His-bundle ablation in 11 patients, incremental ventricular overdrive stimulation studies were performed. The studies, which were spread over a follow-up period of up to 601 days, were carried out invasively with temporary leads as well as noninvasively with the implanted pacemakers and chest wall inhibition. The overdrive pacing rate was increased in steps of 10 beats/min, and the pacing duration was 2 minutes at each level. Ten out of 11 patients had a reliable ventricular escape rhythm; in the remaining patient, consistently no subsidiary pacemaker function was observed up to 10 seconds. In 83% of the studies, incremental ventricular overdrive stimulation caused progressive suppression of ventricular impulse formation with exponential increase in ventricular recovery time and progressive postrecovery subsidiary pacemaker depression. In the remaining 17%, ventricular recovery time showed a heterogeneous response to overdrive stimulation--as possible cause alterations in the sympathetic tone and limitations attributable to the method used are discussed. The results of this study demonstrate a rate-dependent overdrive suppression of subsidiary ventricular pacemaker tissue. This can be of clinical importance in patients with complete heart block and rate-adaptive pacemakers because sudden pacemaker failure or temporary pacemaker inhibition at high stimulation rates may cause Stokes-Adams attacks not reproducible at lower pacing rates.
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Schmidinger et al. (1988) studied this question.
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