Introduction
Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common regular supraventricular
tachycardia. Invasive treatment of the arrhythmia consists of the modification of
the slow pathway (SP) using radiofrequency (RF) catheter ablation.
1
Although such treatment has a success rate close to 98%, atrioventricular (AV) block
can occur in up to 2%–3% of patients during or after catheter ablation procedures.
2
“Cardioneuroablation” (CNA) is a method initially proposed to modulate cardiac parasympathetic
tone with the goal of removing or attenuating the functional cardioinhibitory response
in cardioinhibitory syncopes.3, 4, 5
Here, we report on the case of a young patient who was successfully treated using
CNA, after an inadvertent 2:1 AV block, which occurred after a second SP ablation
that resulted in permanent bradycardia with an indication for a pacemaker.
Case report
A 19-year-old woman underwent a SP ablation owing to recurrent AVNRT in a different
center. Two months after the first procedure, she presented with a recurrence of the
arrhythmia. A redo ablation resulted in a permanent 2:1 AV block with a heart rate
(HR) of 46 beats per minute (bpm). Since she was able to tolerate the bradycardia,
which presented as occasional dizziness, but never a syncope, she refused implantation
of a pacemaker at that time. At the age of 25, she expressed a desire to become pregnant
and was referred to our center by a gynecologist, for permanent pacemaker implantation.
Investigations
Initially, a 12-lead surface electrocardiogram (ECG) (Figure 1, left side) and a 24-hour
ECG Holter were performed. The Holter monitoring showed almost permanent type 2 second-degree
AV block with a minimum documented HR of 32 bpm during sleep. The minimum waking HR
was 44 bpm. The maximum documented HR was 162 bpm during exercise. Continuing the
investigation, an atropine test with 2 mg intravenous was performed; during the test,
normal AV conduction was seen, suggesting a functional AV conduction block (Figure 1,
right side).
Figure 1
Initial 12-lead electrocardiogram shows constant 2:1 atrioventricular block (left
side), which ceases after administration of 2 mg atropine intravenously (right side).
Management
The patient was scheduled for CNA complemented with extracardiac vagal stimulation
(ECVS), which was performed under general anesthesia in early February 2019. To avoid
an increase in HR, we commenced the ablation in the antrum of the left superior pulmonary
vein. During the application of RF current, we observed a vagal reaction manifesting
as a complete AV dissociation (Figure 2A). Normal 1:1 AV conduction was first regained
during ablation in the area of the left ridge between the left inferior pulmonary
vein and the auricle (the presumed area of neurovegetative innervation input to the
left atrium accompanying the vein [or ligament] of Marshall, Figure 2B). After this
ablation, the Wenckebach point (WP) was 750 ms. We then continued with the RF applications
at the inferior septum—close to the roof of the coronary sinus—and further shortening
of AH interval was observed from 75 to 45 ms, and WP increased to 460 ms. We finished
the procedure once there was no more AV block during atrial pacing after ECVS (Figure 3)
in both the right and left vagus. Afterward, we administered 2 mg of atropine intravenously,
which alone increased the HR to 100 bpm but had no effect on the WP, which remained
unchanged (ie, 460 ms), suggesting a maximum WP achievable by the cardiac denervation.
Incremental atrial pacing from the coronary sinus catheter up to a cycle length of
200 ms was performed at the very end of the procedure to exclude any proarrhythmogenic
effect of the ablation lesions. No arrhythmias were induced.
Figure 2
A: After ablation in the roof portion of the left superior pulmonary vein (blue arrow),
complete atrioventricular (AV) dissociation occurred. B: Normal 1:1 AV conduction
was first regained during ablation in the area of the left ridge between the left
inferior pulmonary vein and the auricle (blue arrows). A = atrial signal; H = His
bundle signal; V = ventricular signal.
Figure 3
No atrioventricular (AV) block was observed during vagal stimulation (50 Hz, 50 μs
pulses, 5 s), both from the right and from the left jugular vein at the end of the
procedure. A: 1:1 AV conduction was fully reestablished and persisted on the surface
12-lead electrocardiogram during follow-up. B,C: A standard decapolar steerable catheter
(white arrow) introduced high into the jugular vein was used for vagal stimulation
(B: position of the catheter in the right jugular vein; C: position of the catheter
in the left jugular vein).
Follow-up
Two weeks following the procedure, the patient was in normal sinus rhythm and reported
an improvement in her quality of life (QoL), tolerance to physical exercise, and a
complete absence of fatigue and dizziness. Her resting ECG showed normal sinus rhythm:
HR 77 bpm, PQ 160 ms, QRS 90 ms with no repolarization abnormalities.
After 10 months, the patient was still asymptomatic and reported further QoL improvement.
Since February 2019, she has undergone 3 24-hour postprocedural ECG Holter recordings,
with almost identical results: average HR 82–84 bpm, minimum HR 37 bpm (always between
2:00 am and 4:00 am, ie, at night during sleep), maximum HR 180 bpm (waking hours).
No drops of HR below 60 bpm or the presence of Wenckebach-type second-degree AV block
was documented during waking hours. No blood pressure abnormalities were noted during
all in-office follow-ups.
Discussion
To the best of our knowledge, this is the first case report that shows a correction
of an AV block after SP ablation with CNA. Briefly, according to the current guidelines,
treatment for this patient should be a dual-chamber pacemaker.
6
We report here, after a meticulous investigation and thorough discussion with the
patient, a different approach to the treatment of an AV block that avoids pacemaker
implantation into a young patient and all the potentially negative consequences stemming
from the long-term presence of a cardiac stimulation system. The reason why we believed
that CNA would be beneficial in this particular patient was, apart from the positive
reaction to atropine, the fact that no complete AV block was observed after AVNRT
ablation and that the patient was able to regain 1:1 AV conduction during strenuous
exercise. AV conduction impairment definitely had an iatrogenic origin resulting from
structural injury caused by the previous SP ablation, not excessive parasympathetic
tone alone; however, reducing even “normal” parasympathetic tone resulted in normalization
of AV conduction, at least during waking hours and during the majority of the sleeping
cycle. Our case confirms that apart from iatrogenic damage to the AV node area, parasympathetic
tone may also play a role in patients with AV conduction disturbances after SP ablation.
The borderline between reversible or nonreversible changes caused by SP ablation is,
however, definitely difficult to establish. A positive reaction to atropine, a young
age with no structural heart disease, and at least intermittent 1:1 AV conduction
during exercise might be a clue. A recently published case of successfully reduced
parasympathetic tone using CNA, which allowed for a subsequent successful ablation
of the SP in a young patient with AVNRT, suggests that increased parasympathetic tone
may also play a role in AV node conduction disturbances after SP ablation.
7
The initially proposed indication for the CNA procedure was reflex cardioinhibitory
syncope. The ablation procedure is usually performed in both atria, and the targets
are the ganglionated plexi and the atrial parasympathetic innervation. The ablation
can be guided by different methods, including high-frequency stimulation, iodine-123
meta-iodobenzylguanidine imaging (D-SPECT), fractionation mapping, and/or spectral
mapping, but recently the empiric anatomical approach has been increasingly applied
in most procedures. Nevertheless, the extent of CNA procedures should be determined
by its acute efficacy, which is evaluated based on the presence of a cardioinhibitory
reaction during ECVS. During the vagal stimulation, a standard electrode is introduced
either to the right or left jugular vein close to the anatomical position of the vagal
nerve and 50 Hz alternate current of specific waveform and amplitude is applied for
the time of 5 s (see also Figure 3). Vagal irritation usually causes either a complete
asystole (sinoatrial and AV block) or rarely, and only when pacing on the left side,
sinus bradycardia accompanied by complete AV block.
Our endpoint, in this case, was the complete abolishment of a functional AV block
induced by ECVS in both the right and left jugular vein, during atrial pacing, which
prevented the atria from total standstill owing to sinoatrial impulse suppression
when vagally stimulated. We avoided ablating in the anatomical areas correlated with
sinus node vegetative innervation. In this manner, we avoided significant increases
in HR and possible worsening of the AV block in the event that disruption of the AV
node parasympathetic innervation failed.
Conclusion
In this case, CNA was an effective alternative method to definitive pacemaker implantation
for the treatment of AV block with significant functional reserve. The ECVS was easy
to perform and made it possible to define an appropriate endpoint during the procedure
(ie, extensive selective AV node parasympathetic denervation), a fact confirmed by
the complete absence of a response to atropine in the AV nodal territory at the end
of the procedure. We strongly believe that by avoiding pacemaker implantation, we
dramatically improved not only the patient’s QoL but also her long-term prognosis.
Key Teaching Points
•
Cardioneuroablation may be an effective alternative method to definitive pacemaker
implantation for the treatment of atrioventricular conduction disturbances caused
by radiofrequency catheter ablation of the slow pathway in patients with atrioventricular
nodal reentry tachycardia.
•
A significant functional reserve of the atrioventricular node must be determined by
the atropine test prior to cardioneuroablation.
•
The extent of vagal denervation during cardioneuroablation (ie, acute efficacy) should
be evaluated based on the presence of a cardioinhibitory reaction during extracardiac
vagal stimulation.