Changes in Ventricular Repolarization During Post-Vagal Tachycardia in the Young Puppy † 134

Little is known about the dynamic behavior of ventricular repolarization during the acceleration of heart rate that is caused by abruptly withdrawing a vagal stimulus (post-vagal tachycardia, PVT). We measured changes in left ventricular epicardial monophasic action potential durations in 14 chloralose-anesthetized young puppies (mean [±SD] age 28.6±18.6 days) during PVT. Changes in action potential duration at 90% repolarization (APD₉₀) were plotted as a function of (the decreasing) cardiac cycle length during PVT, induced by withdrawal of an 8 Hz vagal stimulation train. Sinus cycle length decreased from a baseline of 311±30 milliseconds (ms) to 236 ±27 ms during PVT. The APD₉₀- cycle length relationship during PVT was nearly horizontal (slope = 0.08±0.09), indicating that there was little or no shortening of APD₉₀ with shortening of cardiac cycle length. In contrast, when cardiac cycle length was shortened by two other mechanisms, rapid atrial pacing and an infusion of isoproterenol, over cycle length ranges that were within 10 ms of those achieved during PVT, APD₉₀ progressively decreased as a function of decreasing cardiac cycle length. The slope of the APD₉₀ - cycle length relationship during rapid atrial pacing was 0.22±0.09 (P < 0.01 vs. PVT). The greatest cycle length-dependent shortening of APD₉₀ occurred during the isoproterenol infusion (slope = 0.44 ±0.17, P < 0.01 vs. PVT). Thus, in the young puppy dynamic adaptation of ventricular repolarization to changes in cardiac cycle length is attenuated during PVT. New concepts concerning the mechanism(s) of PVT, including a primary facilitation of calcium influx into the cell, may be consistent with these observations. A complete understanding of parasympathetic regulation of cardiovascular function must include an understanding of the effects of withdrawal of a vagal stimulus, as well as the primary effects of the vagal stimulus itself.