When a SVT was induced, the protocol was
stopped. In the absence of tachycardia induction,
isoproterenol (0.02 to 1 μg/min) was infused then
to increase the sinus rate to at least 130 beats/min.Atrial pacing was repeated and programmed atrial
stimulation was performed at a cycle length of
400 ms.
Diagnosis of SVT was confirmed by the EPS.
The mechanism of SVT was determined
according to the method of induction, the relation
of atrial and ventricular activation at the onset of
tachycardia and during tachycardia, the sequence
of retrograde atrial activation, and, if necessary,
the effect of premature extrastimulus during SVT.
The SVT was classified as typical AV nodal reentry
within the atrioventricular node (atrioventricular
node reentry tachycardia [AVNRT]) or atypical
AVNRT or reentry within a concealed accessory
atrioventricular connection (atrioventricular reentry
tachycardia [AVRT]).
Atrial vulnerability was defined as the induction
of an AF lasting more than 1 minute during
the EPS.
Catheter ablation of slow pathway or concealed
AP was performed in 843 patients generally
several months after initial evaluation. Ablation
was performed at the time of the study in only
27 patients. Twenty-four-hour monitoring was
systematic after ablation. Antiarrhythmic drugs
and/or β-blockers were interrupted after ablation.
Most of remaining patients were not chronically
treated, because tachycardias were not frequent or
stopped with vagal maneuvers or acute treatment
with antiarrhythmic drug.
The patients were followed from 1 month to
10 years (mean 2.6 ± 2.5 years). Sixty-five were
lost of view after 1 year of follow-up. We collected
information in our database or records of patients
in other hospitals, calling the general physician or
patients themselves.