title: Effect of stimulus intensity on atrial refractoriness and sinus node recovery.
abstract: BACKGROUND
  Prior studies of sinus node function in man stated that the stimulus intensity of overdrive pacing has no effect on the response of the sinus node to overdrive suppression; however, data documenting these statements were lacking. Previous studies have also suggested that drive train stimulus intensity can alter ventricular refractoriness, but similar studies have not been performed on the human atrium. The purpose of this study was to evaluate the effects of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time.
  
  
  RESULTS
  The effect of drive train stimulus intensity on atrial effective refractory period and sinus node recovery time was studied in 42 patients undergoing clinical electrophysiologic tests. The atrial effective refractory period was shorter at 10 mA (221 +/- 20 msec) and 5 mA (232 +/- 25 msec) than at a drive train stimulus intensity of 1.5 times late diastolic threshold (248 +/- 24 msec, P < 0.05 for pairwise comparison). The sinus node recovery time did not demonstrate a similar effect in the baseline state, following beta-adrenergic blockade, or following combined parasympathetic and beta-adrenergic blockade. However, following isolated parasympathetic blockade with atropine, the corrected sinus node recovery time shortened from 88 +/- 51 msec at 1.5 times late diastolic threshold to 48 +/- 55 msec at 10 mA (P < 0.05). Significant variability was present in sinus node recovery time measurements at baseline and following beta blockade; this variability decreased following parasympathetic blockade.
  
  
  CONCLUSIONS
  These data suggest that drive train stimulus intensity can affect the electrophysiologic properties of sinus node and atrial tissue. This effect appears to be mediated by local catecholamine and acetylcholine release and provides further evidence that the interaction between pacing stimuli and the cardiac autonomic system may need to be considered in evaluating electrophysiologic effects.
authors.affiliation: Department of Medicine, Northwestern University School of Medicine, Chicago, Illinois.
authors.forename: F A
authors.initials: FA
authors.lastname: Ehlert
authors.forename: R S
authors.initials: RS
authors.lastname: Damle
authors.forename: J J
authors.initials: JJ
authors.lastname: Goldberger
authors.forename: A H
authors.initials: AH
authors.lastname: Kadish
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D016275:Atrial Function / Q000502:physiology*; D001341:Autonomic Nervous System / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D012849:Sinoatrial Node / Q000503:physiopathology*