Effect of site of pacing on dispersion of refractoriness

Abstract

The variation in dispersion of ventricular refractoriness with different sites of pacing was measured in 11 patients not taking antiarrhythmic drugs. Dispersion of refractoriness between 3 right ventricular sites was determined at constant paced cycle lengths (S 1S 1. Refractoriness to ventricular extrastimulation (S 2 using atrial pacing vs “clinical” pacing (drive or S 1 at the right ventricular apex) vs the conventional measurement of dispersion (S 1 at the site of S 2 was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S 2. Dispersion of ERP was always wider using clinical pacing (65.4 ± 26 ms [± standard deviation]) than atrial pacing or traditional drive (20.4 ± 14 and 19.1 ± 10 ms, p < 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 ± 35 vs 21.8 ± 14 and 17.3 ± 13, p < 0.011). In 2 patients with left bundle branch block these differences were most striking. Clinical pacing foreshortened FRP relative to ERP (FRP shorter than ERP by an average 12.5 ms at nonapical sites) but this did not induce tachycardias, perhaps because FRP was still longer than the shortest V 1V 2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p < 0.05). With atrial pacing there is less dispersion of refractoriness than with clinical ventricular pacing, although this difference is not appreciated when dispersion is measured in the conventional manner.