EP procedure
Antiarrhythmic medications were discontinued approximately 5 half-lives prior to the procedure. An EPS was performed as previously described31. In general, the procedure was performed under sedation with ultrasound guided femoral venous access for the deflectable decapolar CS, quadripolar His and the ablation catheters. A retrograde study with single ventricular extra stimulus testing was performed first followed by the antegrade study with a single atrial extra stimulus. A reproducible increase in the last atrial extra stimuli -His (A1A2/A2H2) interval of 50 milliseconds or greater in response to a decrease in the last A-A coupling interval of 10 milliseconds was defined as dual AV nodal conduction or an AH ‘jump’. Next, atrial then ventricular pacing to Wenckebach AV nodal conduction was performed. At that stage if AVNRT was non inducible then sensed double and/or triple atrial extra stimuli in 10msec increments was completed. Testing continued until AVNRT was sustained. If sustained tachycardia could not be induced, intravenous isoproterenol (1, 2 or 4mcg/minute) was administered and the pacing manoeuvres repeated. AVNRT was diagnosed using established criteria29, 32, 33
Ablation was performed in sinus rhythm. A non-irrigated 4mm deflectable solid tip ablation catheter was used with a long vascular sheath to facilitate stability. The region of slow pathway was identified using a combination of anatomic and electrogram characteristics under fluoroscopic guidance7, 31, 34-36 with 3 dimensional mapping when available (Figure 1). The target sites typically had a multi component atrial electrogram with an AV ratio of < 0.5. Ablation was performed with a maximum power of 50W and temperature limit set to 60 degrees Celsius. Ablation generally commenced at the posterior septal tricuspid annulus (TA) immediately adjacent to the inferior margin of the ostium of the coronary sinus in the region of the triangle of Koch. Subsequent RF applications progressed superiorly if initial ablation attempts did not result in junctional acceleration. JR was defined as a QRS complex identical to that of the sinus beat without evidence of atrioventricular (AV) conduction. RF was discontinued after 30 seconds if no junctional rhythm occurred. RF was also discontinued immediately if any degree of AV or (Junctional beat-atrial) JA block occurred or in the presence of rapid junctional rhythm (<350ms). Every ablation was included in the analysis if there were any JR during ablation or a lesion duration of ≥5 seconds regardless of the presence of JR. After each RF application, the EP manoeuvres responsible for inducing AVNRT were repeated. Further testing was repeated on isoproterenol if AVNRT was non inducible. Acute procedural success was defined by (1) complete loss of slow pathway conduction or (2) by the presence of no more than a single AV nodal echo beat (slow pathway modification). Isoproterenol was administered after every ablation if it had been required for arrhythmia induction prior to ablation or persistent AV nodal echo beats were present after ablation. Following successful RF application, EP testing was repeated on isoproterenol in all patients throughout a mandatory 20-minute waiting period. If there was recurrence of inducible tachycardia or more than one echo beat during the waiting period, additional ablation was performed as per the protocol.
For each RF application: ablation duration, cycle length of JR, the presence of AV and VA conduction during JR and any change in AV conduction following ablation were recorded.
Antiarrhythmic therapy was not recommenced after the ablation procedure. Patients were followed up prospectively for a minimum of 6 months. Recurrence was defined as documented AVNRT lasting >30seconds occurring at any time after the ablation procedure. Clinical symptoms of palpitations were investigated with a Holter monitor in addition to serial ECG’s and provision of an Alivecor monitor.