Effect of site of pacing on dispersion of refractoriness.
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 (S1S1). Refractoriness to ventricular extrastimulation (S2) using atrial pacing vs "clinical" pacing (drive or S1 at the right ventricular apex) vs the conventional measurement of dispersion (S1 at the site of S2) was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S2. 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 less than 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 +/- 35 vs 21.8 +/- 14 and 17.3 +/- 13, p less than 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 V1V2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p less than 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.
D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D002037:Bundle-Branch Block / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D004558:Electric Stimulation / Q000379:methods; D004562:Electrocardiography; D006325:Heart Atria / Q000503:physiopathology; D006352:Heart Ventricles / Q000503:physiopathology; D006801:Humans; D013997:Time Factors