The aim of our work was to evaluate the inducibility of atrial fibrillation in a group of patients with atrioventricular junctional reentrant tachycardia and to compare it with that of patients with a Kent-type ventricular pre-excitation (Wolff-Parkinson-White syndrome) and a control group. One hundred and twenty-five subjects were separated into groups. Group 1 comprised 49 Wolff-Parkinson-White patients, with a mean age of 26.4, range 10-66 years; group 2, 51 patients with atrioventricular junctional reentrant tachycardia inducible by transoesophageal atrial stimulation and/or clinically documented, with a mean age of 43.4, range 16-78 years; group 3, 25 control subjects with a mean age of 26.4, range 13-76 years. Each subject underwent atrial transoesophageal stimulation with the following protocol: programmed atrial stimulation with 1 and 2 stimuli during atrial pacing of 100.min-1 and 150.min-1; atrial stimulation for 10 s at a rate of 200-300-400-500-600.min-1 with intervals of 10 s between stimulations, five successive 'ramp-up' atrial stimulations for 9 s with the rate increasing from 100 to 800.min-1 with intervals of 10 s between stimulations. The end point was the completion of the protocol or induction of sustained atrial fibrillation (> 1 min). The chi-square test was used for statistical analysis. Our results showed that in group 1 atrial fibrillation was induced in 27/49 patients (55.1%); this was sustained in 13/49 (26.5%) and non-sustained in 14/49 (28.5%); in group 2, atrial fibrillation was induced in 22/51 patients (43.0%); it was sustained in 7/51 (13.7%) and non-sustained in 15/51 (29.4%); in group 3, sustained atrial fibrillation was not induced in any subject and in only one subject was a non-sustained atrial fibrillation (4 s) induced. The chi-square test showed that group 2 vs group 1 were non-significant, while group 2 vs group 3 and group 1 vs group 3 were significant (P < 0.003 and P < 0.0007, respectively). Therefore group 2 patients showed a greater atrial vulnerability in comparison to the control subjects and a similar vulnerability to group 1 patients. It is possible that the greater atrial vulnerability in the patients of group 2 was due to the double nodal pathway.

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