Key result
Patients with atrioventricular junctional reentrant tachycardia had a significantly higher rate of induced atrial fibrillation compared to controls (43.0% vs 4.0%; P<0.003).
Why the study?
Does transoesophageal atrial stimulation reveal greater atrial vulnerability in patients with atrioventricular junctional reentrant tachycardia compared to controls?
Observational (n=125)
Does transoesophageal atrial stimulation reveal greater atrial vulnerability in patients with atrioventricular junctional reentrant tachycardia compared to controls?
Patients with atrioventricular junctional reentrant tachycardia exhibit greater atrial vulnerability to induced atrial fibrillation than controls, similar to patients with Wolff-Parkinson-White syndrome.
AVJRT patients show greater atrial vulnerability to induced AF; cross-sectional data leaves open implications for AF risk stratification.
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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D’Este et al. (1995) conducted an observational in Atrioventricular junctional reentrant tachycardia and Wolff-Parkinson-White syndrome (n=125). Atrioventricular junctional reentrant tachycardia vs. Healthy controls was evaluated on Induction of atrial fibrillation (sustained or non-sustained) (p=< 0.003). Patients with atrioventricular junctional reentrant tachycardia had a significantly higher rate of induced atrial fibrillation compared to controls (43.0% vs 4.0%; P<0.003).
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