The maximum effect of an increase in rate on human ventricular refractoriness.

The purpose of this study was to determine the maximum shortening of ventricular refractoriness that occurs following an increase in rate and to quantitate the duration of ventricular pacing required to obtain this maximum shortening of refractoriness. The subjects of the study consisted of 41 patients who underwent a clinically indicated electrophysiologic study. Ventricular refractory periods were measured with an extrastimulus (S2) at basic cycle lengths of 600 and 400 ms by Method A (8 beat basic drive trains and 4 second intertrain paue and Method B (drive train duration of 3 minutes, then an S2 after every eighth basic drive beat, with no pause after the S2). In 23 subjects, the mean ventricular effective refractory period determined by Method B was 12 +/- 7 ms (+/- standard deviation) shorter than when determined by Method A at a basic drive cycle length of 600 ms (p less than 0.0001) and 33 +/- 9 ms shorter at a basic drive cycle length of 400 ms (p less than 0.001). In these 23 subjects, the drive train duration required for maximum shortening of ventricular refractoriness was estimated by counting the number of drive train beats preceding ventricular capture by an S2 inserted after every fourth basic drive beat at a coupling interval fixed at 5 ms longer than the ventricular effective refractory period determined in that subject by Method B. The mean number of basic drive beats preceding capture by S2 was 114 +/- 84 beats at a basic drive cycle length of 600 ms and 233 +/- 85 beats at a BDCL of 400 ms. In six subjects the ventricular effective refractory period was measured by Methods A and B before and after autonomic blockade with propranolol and atropine, and the amount of shortening in the ventricular effective refractory period with Method B was not affected by autonomic blockade. In conclusion, the basic drive train has a cumulative effect on ventricular refractoriness in humans, and a drive train duration substantially longer than 50 beats often is required to obtain the maximum shortening of ventricular effective refractory period after an increase in rate. Therefore, ventricular effective refractory periods determined conventionally using 8 beat drive trains and a 4 second intertrain pause often may be overestimates of the actual ventricular effective refractory period. The shortening of ventricular refractoriness with long drive train durations is probably related to a prolonged duration of pacing required to obtain a steady-state action potential duration after an increase in rate.