Fast/Slow Atypical AVNRT: Differentiating Subforms

AV nodal reentry tachycardia (AVNRT) is the most common form of SVT, making up approximately 56% of SVTs brought into the EP lab for ablation.¹ Within the classification of AVNRT are three subsets: typical slow/fast, and two mechanisms of atypical (slow/slow and fast/slow). All three categories are labeled with the antegrade limb first and the retrograde limb second. Of these three subsets, typical slow/fast makes up 94%, atypical fast/slow 4%, and atypical slow/slow 2%.² In typical AVNRT, an antegrade slow AV nodal pathway is categorized by a “jump” (a 50 msec increase in A2-H2 following a 10 msec decrease in atrial coupling interval A1-A2).³ In patients without an abrupt 50 msec increase, an A2-H2 greater than 200 msec can also justify labeling as an antegrade slow pathway.⁴ Of the two forms of atypical AVNRT, differentiation can be made by looking at the antegrade conduction during tachycardia. In fast/slow AVNRT, the AH in tachycardia should be <200 msec. In slow/slow AVNRT, the AH during tachycardia should be >200 msec.² There are several articles that have been published on the differentiation of these subtypes utilizing various criteria; for the purpose of this article, we chose this simple method of measuring AH during tachycardia.

 

In this article, we present a case describing diagnosis and treatment of AVNRT, with the specific mechanism being fast/slow atypical AVNRT.  

An 81-year-old female was referred by a cardiology group for evaluation of sick sinus syndrome and potential need for permanent pacemaker implantation. For years, the patient had a history of palpitations, which increased in frequency over the last six months. Her palpitations were associated with dyspnea, occurred at times of minimal exertion or “when changing positions”, and manifested on a daily basis. The symptoms had forced the patient to change her lifestyle, and she voiced her displeasure in no longer being able to work in her garden. A 12-lead ECG in the office showed sinus rhythm with normal PR interval, no sign of pre-excitation, and occasional PVCs.

 

A 24-hour Holter monitor was ordered, which showed numerous runs of narrow complex tachycardia that were often both initiated and terminated with PVCs. We started the patient on metoprolol, which did not help her symptoms; titrating it up, her sinus rates were in the 40s. After discussion with the patient, she agreed to an EP study with possible radiofrequency ablation.

 

The Holter strips (Figures 2-3) show initiation of a long RP tachycardia and termination by PVCs. This supported the idea of this tachycardia possibly being an AVNRT.

 

The ECG obtained prior to the EP study showed a narrow complex long RP tachycardia at approximately 140 bpm. The P wave morphology was noted as having the potential of being retrograde (-) in the inferior leads. From the ECG, we could also note an iso P wave in lead I, a iso/+ in V1 transitioning to negative at V2, and positive P wave in AVL. This morphology was noted as potentially originating from the area of the coronary sinus (CS) ostium.8 (Figure 4)

 

The patient was brought to the EP lab, and both femoral regions were prepped for the procedure using standard sterile technique. Conscious sedation was initially withheld, opting for only the use of a local anesthetic of lidocaine for femoral access until the tachycardia was induced.

 

Venous access was obtained in both groins using the percutaneous approach, and four diagnostic catheters were inserted for the baseline EP study of the high right atrial (HRA), right ventricular apex (RVA), His, and CS regions. 

 

The EP study began with stimulation from the HRA; programmed electrical stimulation with single extrastimuli revealed concentric and decremental ventricular activation with no jump or signs of dual AV nodal physiology. Retrograde pacing from the RV catheter was then performed, revealing concentric and decremental atrial activation, and a retrograde jump at 600-310 msec. Burst pacing from the ventricle was performed, and while pacing at 400 msec, a long RP tachycardia was induced. The tachycardia had an AH of 150 msec, HV of 59 msec, VA of 212, and tachycardia cycle length of 415 msec (Figure 5). Retrograde activation was noted to be concentric with earliest atrial activation at the His catheter. (Proximal electrode pair of the CS catheter was noted to be well within the coronary sinus, and did not give a good representation of timing at the ostium.) If positioned close to the ostium, the CS catheter could sometimes appear earlier than the His. His synchronous PVC was delivered, revealing no advancement of the subsequent VA time. The failure of the PVC to advance the following atrial signal was not definitive proof of the absence of an accessory pathway.⁵ Next, entrainment was performed from the ventricle. Burst pacing at 400 msec from the RV catheter showed entrainment of the atrium, and yielded a VAV response. This finding confirmed an AV reentrant mechanism and excluded atrial tachycardia as a mechanism.⁶ Tachycardia was terminated with ventricular burst pacing at 300 msec. A final test of Para-Hisian pacing was performed to determine if there was presence of a septal accessory pathway. Para-Hisian pacing yielded an increase of S-A (stim to A) time of 60 msec, which confirmed the lack of a septal accessory pathway.⁷ With these pacing maneuvers complete, we were comfortable with the diagnosis of AVNRT, and the specific mechanism being fast/slow atypical AVNRT. Referring back to the measurements during tachycardia, AH of 150 msec would tell us the antegrade limb is the fast pathway. Also of note, we were never able to show any evidence of antegrade slow pathway conduction, on or off isoproterenol infusion. The VA interval of 212 msec during tachycardia would suggest the retrograde limb is a slow AV nodal pathway. Attempts at re-induction demonstrated the arrhythmia was easily inducible with ventricular burst pacing at or around 400 msec. At this point, conscious sedation (midazolam and fentanyl) was given for patient comfort.

 

Isoproterenol infusion was administered, at 1-2 mcg/min, and AV nodal conduction properties were re-evaluated. On isoproterenol, antegrade AV nodal conduction still revealed no jump or sign of dual AV nodal physiology. A long RP tachycardia was easily induced with programmed electrical stimulation from the HRA catheter. The induced arrhythmia had the same activation sequence and response to pacing maneuvers as the arrhythmia induced off isoproterenol, just a slightly shorter CL of 405 msec. Ventricular stimulation showed the same easily inducible long RP tachycardia, both with burst pacing and single extrastimuli pacing. It was decided to continue with slow pathway ablation for this fast/slow atypical AVNRT, and isoproterenol was discontinued.

 

Three-dimensional mapping was utilized during tachycardia using the EnSite Precision mapping system (Abbott), and a localized activation map was created of the retrograde atrial activation.   Retrograde slow pathway activation was shown to be earliest just anterior to the lip of the coronary sinus. It should be noted that the earliest retrograde activation site should not be the primary criteria for targeting RF applications, but a more traditional anatomic slow pathway location should be utilized.² Signals at this location were noted to have a good A-V relationship for slow pathway ablation, with no presence of a His bundle signal (Figure 6). Radiofrequency (RF) therapy was administered at this location using a Safire 7 Fr 4 mm tip medium curve ablation catheter (Abbott) for 60 seconds at 50 watts, with a programmed maximum temperature of 55 degrees. The 55 degrees was achieved with approximately 30W of energy delivery, and impedance was monitored throughout the ablation. Junctional ectopy was achieved with this RF application, and an impedance drop of 8 ohms was noted. Two bonus lesions were given at the successful site, with eventual cessation of junctional ectopy.

 

Post-ablation AV nodal conduction and possible presence of the retrograde slow AV nodal pathway were assessed, revealing no changes in antegrade AV nodal conduction and no signs of the retrograde slow pathway. A 30-minute wait period was observed from the time of the last lesion given. Isoproterenol infusion was re-initiated at 2 mcg/min, and the patient was once again evaluated for retrograde slow pathway conduction or induction of tachycardia, with no signs of either.

 

When the patient came back for follow-up, she was enjoying her life again, with no recurrent symptoms of PSVT.

 

Disclosures: The authors have no conflicts of interest to report regarding the content herein.