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.