We report results of follow-up transesophageal electrophysiologic studies in 35 infants seven to 27 months old (mean, 12 months) in whom paroxysmal atrial tachycardia (PAT) using an accessory atrioventricular (AV) connection had been previously evaluated by transesophageal study in the first 2 months (mean, 14 days) of life. No infants were receiving antiarrhythmic drug therapy at the time of follow-up study. To evaluate AV induction and initiate PAT, a standard transesophageal pacing protocol was used: single extrastimuli in sinus rhythm, incremental pacing to second-degree AV block, and burst pacing at cycle lengths near those resulting in second-degree AV block. If PAT was not initiated during the baseline period, the protocol was repeated during the infusion of isoproterenol and after administration of atropine. At follow-up study, PAT was reinitiated in 24 of 35 (68%) infants, six of whom had exhibited recent spontaneous recurrence of PAT. AV nodal function did not differ in those with and those without inducible PAT. However, when initial and follow-up studies were compared, changes in antegrade conduction of the accessory AV connection were observed, since only five of 10 infants with preexcitation at initial study continued to exhibit preexcitation at follow-up study (1/5 infants only after isoproterenol). Additionally, changes in retrograde conduction of the accessory AV connection were observed; the ventriculoatrial interval in PAT induced at follow-up study increased by 20 to 40 msec in eight of 24 infants and 50 to 80 msec in five of 24 infants compared with the interval at initial study. Thus, in 24 of 35 infants with PAT in the first 2 months of life, susceptibility to inducible PAT persisted whether or not spontaneous PAT was observed. Since AV nodal function was similar in infants with and those without inducible PAT, the loss of susceptibility to both inducible and/or spontaneous PAT may in part be due to observed developmental changes in electrophysiologic properties of accessory AV connections.