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Europace (2000) 2, 181–185
doi:10.1053/eupc.1999.0087, available online at http://www.idealibrary.com on
CASE REPORT AND LITERATURE REVIEW
Autonomic effects of radiofrequency catheter ablation
F. Duru, U. Bauersfeld and R. Candinas
Cardiac Arrhythmia Unit, University Hospital of Zurich, Zurich, Switzerland
Radiofrequency (RF) catheter ablation has become the
treatment of choice for a variety of supraventricular tachycardias. Autonomic dysfunction may occur during application of RF current; these abnormalities resolve quickly
when current delivery is terminated. We present a case of
sinus node arrest and AV block in a 69-year-old woman
induced by RF catheter ablation of an AV nodal slow
pathway. The proposed mechanisms are a Bezold-Jarischlike phenomenon or paradoxical activation of cardiac C
fibres by direct neural sympathetic stimulation or RF-
induced myocardial injury. Based on a review of previously
published reports, autonomic effects of RF ablation are
discussed.
(Europace 2000; 2: 181–185)
2000 The European Society of Cardiology
Introduction
Cardiac asystole, an extreme manifestation of neurocardiogenic reaction, may also rarely occur during RF
current application. Cases of RF ablation-induced
asystole during ablation of accessory pathways have
been reported previously[7,8]. Profound sinus bradycardia and asystole may also occur during ablation of
pulmonary tissues in patients with paroxysmal atrial
fibrillation[9]. We present a case of sinus node arrest and
AV block with resultant syncope induced during RF
ablation of an AV nodal slow pathway.
Radiofrequency (RF) catheter ablation has been widely
accepted as the treatment of choice for a variety of
supraventricular tachycardias, including atrioventricular
(AV) nodal reentrant tachycardia[1–3]. It is a safe procedure in experienced centres and definitive cure is obtained in the vast majority of cases. A potential, but rare
complication is complete heart block requiring implantation of a permanent pacemaker[4,5]. Selective ablation
of the slow pathway is less likely to be associated with
conduction disturbances, and therefore it has been the
favoured approach in most centres. Nevertheless, transient AV block or abrupt slowing of the sinus node
suggesting autonomic dysfunction may occasionally
occur during RF current application to sites remote
from the sinus node and the AV node[6]. Direct stimulation of parasympathetic fibres travelling to the sinus
node and the AV node, or alternatively, stimulation of
autonomic receptors that by reflex mediate a change in
autonomic tone affecting the sinus node and AV node
function are among the proposed mechanisms for these
observations[6].
Manuscript submitted 8 June 1999, and accepted 21 December
1999.
Correspondence: Firat Duru, MD, Cardiac Arrhythmia Unit, University Hospital of Zurich, Rämistr. 100, Zurich, 8091 Switzerland.
1099–5129/00/020181+05 $35.00/0
Key Words: Radiofrequency ablation, AV nodal reentrant
tachycardia, slow pathway, asystole, autonomic dysfunction.
Case history
A 69-year-old female patient with AV nodal reentrant
tachycardia was referred to our institution for RF
catheter ablation. The patient had experienced syncopal
episodes during early adulthood, suggestive of neurocardiogenic syncope, and had suffered from recurrent,
drug-resistant palpitations for more than 10 years. She
had undergone RF catheter ablation 4 years before
which revealed an AV nodal reentrant tachycardia with
a rate of 125 beats.min 1 that was no longer inducible
after ablation of the slow pathway. Administration of
isoprenaline during this procedure resulted in presyncope due to transient paradoxical slowing of the
sinus rate (PP intervals up to 2 s) and transient complete AV block with a ventricular escape rhythm of
32 beats.min 1 during atrial pacing. The ablation
2000 The European Society of Cardiology
182
F. Duru et al.
12·5 mm.s–1
2000 ms
6–aVF
7–V1
5785 ms
12–V6
14–HRA
16–HIS
28–Abl.p
End RF
Begin RF
27–Abl.
Figure 1 Progressive slowing of the sinus node is observed during initial RF current delivery for AV nodal
slow pathway ablation. (HRA=high right atrium, Abl=ablation, p=proximal.)
procedure was considered successful and antiarrhythmic
medications were withdrawn.
Despite initial success, the patient reported palpitations several months after discharge. Her physical
examination and the surface 12-lead ECG were normal.
After informed consent had been obtained, the patient
was admitted to the electrophysiological (EP) laboratory
in the fasting, non-sedated state. Three multipolar electrode catheters (2-mm interelectrode space) were introduced from the right femoral vein and placed in the right
atrium, His bundle area, and right ventricle. The clinical tachycardia with a rate of 120 beats.min 1 was
induced during placement and manipulation of the
electrode catheters and was also easily inducible during
baseline EP study. The diagnosis of AV nodal reentrant
tachycardia was established by tachycardia initiation
dependent on an A-H delay of 70 ms and the earliest
retrograde activation in the His bundle electrogram.
Termination could be achieved easily with atrial or
ventricular pacing. A 7-French deflectable quadripolar
ablation catheter with a 4-mm tip and 2-mm interelectrode distance (Sulzer Osypka Cerablate Plus TTwin
745, Grenzach-Wyhlen, Germany) was introduced. The
tip of the ablation catheter was positioned along the
posteroseptal right atrium, close to the tricuspid annulus, where the His deflection was no longer visible and
the ratio of atrial to ventricular deflection was below 1.
RF energy was applied with an Osypka HAT 300
Europace, Vol. 2, April 2000
generator (Grenzach-Wyhlen, Germany) between the
distal electrode of the ablation catheter and the cutaneous patch electrode placed over the left scapula.
During initial delivery of the temperature-controlled RF
current, progressive slowing of the sinus node was noted
(Fig. 1). The second RF application in the same region
during tachycardia resulted in sinus node arrest with
resultant syncope after approximately 7 s of RF current
delivery (Fig. 2). Atrial pacing showed complete AV
block initially which recovered after approximately 10 s.
Administration of atropine abolished the occurrence of
sinus arrest and AV block during RF current delivery in
the same region. The subsequent two attempts at the
same location resulted in slowing of the sinus rate. The
patient reported no discomfort or pain during the whole
procedure. Careful assessment of sinus nodal and AV
nodal function following asystole revealed no abnormalities. There was no detectable sudden increment in
the A-H interval and the tachycardia was no longer
inducible. The patient remained free of tachycardia and
syncope recurrences 1 year after the procedure.
Discussion
It is known that autonomic dysfunction may occur as a
consequence of RF catheter ablation of a variety of
supraventricular tachycardias[6]. Acute effects during
Autonomic effects of radiofrequency catheter ablation
12·5 mm s–1
183
2000 ms
6–aVF
7–V1
10 374 ms
12–V6
Atrial pacing
14–HRA
16–HIS
28–Abl.p
End RF
27–Abl.
Figure 2 Sinus node arrest is noted after 7 sec of RF current delivery. Atrial pacing is performed which
shows complete AV block. The patient develops asystole with resulting syncope. After approximately 10 s,
AV block resolves, followed by gradual recovery of the sinus node.
application of RF current include slowing of the sinus
rate or transient AV block which usually resolve quickly
when current delivery is terminated. Transient AV block
may occur due to mechanical or RF injury in the
junctional area[10–12]. Application of RF current along
the tricuspid or mitral annulus, at sites distant from both
the sinus node and the AV node, may also be associated
with profound sinus bradycardia or transient AV block,
suggestive of autonomic dysfunction[6]. It has been
shown that atrial tissue in close proximity to the AV
rings has a high concentration of autonomic nerve
fibres. Therefore, direct stimulation of parasympathetic
nerve fibres travelling from the site of RF application to
the sinus node and the AV node and alternatively, a
reflex-mediated change in autonomic tone are among
the proposed mechanisms[6].
In contrast to the above-mentioned transient effects,
RF ablation may create chronic AV block or cause a
long-lasting increase in sinus rate[13–15]. The precise
mechanism for inappropriate sinus tachycardia, defined
as a resting sinus rate >100 beats.min 1 in the absence
of physiological precipitants, is unknown. A study based
upon spectral analysis of heart rate variability showed a
decrease in high-frequency components immediately
after an ablation procedure, suggestive of reduced parasympathetic tone[16]. The abnormalities of heart rate and
of heart rate variability resolved 1 to 6 months after
ablation, with reappearance of the high frequency parasympathetic component, probably due to reinnervation.
These changes were most obvious in patients undergoing
AV node modification and ablation of a posteroseptal
accessory bypass tract and were related to a possible
concomitant destruction of vagal inputs[16,17].
Transient asystole, preceded by a profound slowing of
the sinus rate has been reported during RF ablation of
accessory pathways[7,8]. Schläpfer et al. presented a case
of sinus bradycardia followed by an 8-s asystole induced
by RF current application via the coronary sinus for
ablation of a left posteroseptal accessory pathway[7].
Tsai et al. reported a case of asystole for 5·5 s during RF
application on the ventricular aspect of the mitral
annulus for a left anterolateral accessory pathway[8].
Similar to the previous case, there was progressive
slowing of the sinus rhythm. Asystole was terminated by
right ventricular pacing and, after 15 s, the sinus rate
gradually increased to the pre-ablation level. Both
patients experienced near-syncope during the transient
asystole. A reflex-mediated mechanism, the BezoldJarisch phenomenon, was proposed as an explanation in
both cases. This inhibitory reflex originating in cardiac
sensory receptors with vagal afferents produces both an
increase in parasympathetic activity and a decrease in
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F. Duru et al.
sympathetic activity resulting in bradycardia, vasodilation and hypotension[18–22]. More recently, similar
observations have been made during RF ablation of the
pulmonary vein tissues in patients with paroxysmal
atrial fibrillation[9].
The anatomy of the autonomic innervation of the
heart is complex[23]. The sympathetic and parasympathetic innervation of the sinus node and the AV node
follow different courses. Parasympathetic pre-ganglionic
neurones, located in the medulla oblongata of the brain
stem, send fibres to the heart through the vagus nerves.
Within the heart itself, pre-ganglionic fibres destined
to innervate the sinus node terminate in the pulmonary vein fat pad, whereas those that innervate
predominantly the AV node terminate in the inferior
vena cava–inferior left atrial fat pad. Parasympathetic
denervation by surgical dissection of the fat pads does
not influence sympathetic control of sinus rate and AV
nodal conduction. The human heart contains a variety
of morphologically distinct nerve terminals that are
distributed more widely than has been described in
experimental animals[24]. Coronary sinus and epicardial
nerve terminals arise only from myelinated nerve
fibres, whereas endocardial terminals arise from either
myelinated or non-myelinated fibres. The nonmyelinated endocardial nerve terminals are believed to
be responsible for reflex vasodilation and bradycardia,
and correspond to those described electrophysiologically
as C-fibres. In addition to intramyocardial pressure,
C-fibres may also be activated by nicotine, catecholamines, neural sympathetic stimulation and myocardial
infarction[25]. The unmyelinated afferent C-fibre terminals were found to be numerous in areas of the roof of
the left atrium, around the four pulmonary veins, the
lateral wall of the right atrium, and the posterior wall of
the left ventricle[24]. Thus, profound sinus bradycardia and asystole occurring when RF energy was
delivered to the regions described in the previously
published reports[7–9] is concordant with the known high
concentration of vagal afferent receptors in these areas.
Our case is, to the best of our knowledge, the first
reported case of reflex-mediated sinus node arrest and
AV block induced by RF ablation of an AV nodal slow
pathway. A reflex mechanism in our case is suggested by
the fact that asystole duration was longer than that of
direct stimulation of efferent vagal fibres, which would
only last for 1 to 2 s after cessation of stimulation[26].
Assessment of the sinus nodal and the AV nodal
function following termination of asystole revealed no
abnormalities, suggesting that the transient sinus arrest
and the AV block had been the result of a change in
autonomic tone. Atropine abolished reoccurrence of this
phenomenon during subsequent RF applications, possibly due to its counteracting effects on the efferent
parasympathetic limb of the reflex arc. The patient
experienced no pain during RF current delivery, which
could provoke a central type vasovagal response[27,28].
Previous history of syncopal episodes and a decrease in
heart rate following isoprenaline administration in our
case suggests a mechanism similar to that observed in
Europace, Vol. 2, April 2000
neurocardiogenic syncope, a condition characterized by
a paradoxical withdrawal of sympathetic activity and
an increase in parasympathetic activity possibly in
response to excessive stimulation of ventricular
mechanoreceptors[29–33]. While the efferent limb of the
reflex arc in our case is probably similar to that observed
in neurocardiogenic syncope, the afferent limb was
triggered by RF ablation and not by changes in
intramyocardial pressure.
A Bezold-Jarisch-like phenomenon or paradoxical
activation of cardiac C fibres by direct neural sympathetic stimulation or RF-induced myocardial injury may
be responsible in our case, but given the complexity of
autonomic innervation in human hearts, the above
mentioned causal mechanisms can only be speculative.
However, our case might serve to call attention to the
possibility that a reflex transient sinus node arrest and
AV block may occur during RF ablation of an AV
nodal slow pathway.
References
[1] Naccarelli GV, Shih HT, Jalal S. Catheter ablation for
the treatment of paroxysmal supraventricular tachycardia.
J Cardiovasc Electrophysiol 1995; 6: 951–61.
[2] Kay GN, Epstein AE, Dailey SM, Plumb VJ. Role of radiofrequency ablation in the management of supraventricular
arrhythmias: experience in 760 consecutive patients. J
Cardiovasc Electrophysiol 1993; 4: 371–89.
[3] Akhtar M, Jazayeri MR, Sra J, Blanck Z, Deshpande S,
Dhala A. Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations. Circulation
1993; 88: 282–95.
[4] Chen SA, Chiang CE, Tsang WP, et al. Selective radiofrequency catheter ablation of fast and slow pathways in 100
patients with atrioventricular nodal reentrant tachycardia.
Am Heart J 1993; 125: 1–10.
[5] Hindricks G. Incidence of complete atrioventricular block
following attempted radiofrequency catheter modification of
the atrioventricular node in 880 patients. Results of the
Multicenter European Radiofrequency Survey (MERFS) The
Working Group on Arrhythmias of the European Society of
Cardiology. Eur Heart J 1996; 17: 82–8.
[6] Friedman PL, Stevenson WG, Kocovic DZ. Autonomic dysfunction after catheter ablation. J Cardiovasc Electrophysiol
1996; 7: 450–9.
[7] Schläpfer J, Kappenberger L, Fromer M. Bezold-Jarisch-like
phenomenon induced by radiofrequency ablation of a left
posteroseptal accessory pathway via the coronary sinus.
J Cardiovasc Electrophysiol 1996; 7: 445–9.
[8] Tsai CF, Chen SA, Chiang CE, et al. Radiofrequency
ablation-induced asystole during transaortic approach for a
left anterolateral accessory pathway: a Bezold-Jarisch-like
phenomenon. J Cardiovasc Electrophysiol 1997; 8: 694–9.
[9] Tsai CF, Chen SA, Tai CT, et al. Bezold-Jarisch-like reflex
during radiofrequency ablation of the pulmonary vein
tissues in patients with paroxysmal focal atrial fibrillation.
J Cardiovasc Electrophysiol 1999; 10: 27–35.
[10] Fenelon G, d’Avila A, Malacky T, Brugada P. Prognostic
significance of transient complete atrioventricular block during radiofrequency ablation of atrioventricular node reentrant
tachycardia. Am J Cardiol 1995; 75: 698–702.
[11] Hintringer F, Hartikainen J, Davies DW, et al. Prediction of
atrioventricular block during radiofrequency ablation of the
slow pathway of the atrioventricular node. Circulation 1995;
92: 3490–6.
Autonomic effects of radiofrequency catheter ablation
[12] King A, Wen MS, Yeh SJ, Wang CC, Lin FC, Wu D.
Catheter-induced atrioventricular nodal block during
radiofrequency ablation. Am Heart J 1996; 132: 979–5.
[13] Ehlert FA, Goldberger JJ, Brooks R, Miller S, Kadish AH.
Persistent inappropriate sinus tachycardia after radiofrequency current catheter modification of the atrioventricular
node. Am J Cardiol 1992; 69: 1092–5.
[14] Skeberis V, Simonis F, Tsakonas K, Celiker A, Andries E,
Brugada P. Inappropriate sinus tachycardia following radiofrequency ablation of AV nodal tachycardia: incidence and
clinical significance. Pacing Clin Electrophysiol 1994; 17:
924–7.
[15] Pappone C, Stabile G, Oreto G, De Simone A, Rillo M,
Mazzone P, Cappato R, Chierchia S. Inappropriate sinus
tachycardia after radiofrequency ablation of para-Hisian
accessory pathways. J Cardiovasc Electrophysiol 1997; 8:
1357–65.
[16] Kocovic DZ, Harada T, Shea JB, Soroff D, Friedman PL.
Alterations of heart rate and of heart rate variability after
radiofrequency catheter ablation of supraventricular tachycardia. Delineation of parasympathetic pathways in the
human heart. Circulation 1993; 88: 1671–81.
[17] Geller C, Goette A, Carlson MD, et al. An increase in sinus
rate following radiofrequency energy application in the
posteroseptal space. Pacing Clin Electrophysiol 1998; 21:
303–7.
[18] Von Bezold A, Hirt H. Uber die physiologischen Wirkungen
des Essigsauren Veratrius. Unters Physiol Lab Würtzburg
1867; 1: 75–156.
[19] Jarisch A, Richter H. Die Kreislaufwirkung des Veratrins.
Arch Exp Pathol Pharmakol 1939; 193: 355–71.
[20] Jarisch A, Zotterman Y. Depressor reflexes from the heart.
Acta Physiol Scand 1948; 16: 31–51.
[21] Mark AL. The Bezold-Jarisch reflex revisited: clinical implications of inhibitory reflexes originating in the heart. J Am
Coll Cardiol 1983; 1: 90–102.
185
[22] Hainsworth R. Reflexes from the heart. Physiol Rev 1991; 71:
617–58.
[23] Randall WC, Ardell JL. Nervous control of the heart:
Anatomy and pathophysiology. In Zipes DP, Jalife J,
eds. Cardiac Electrophysiology: From Cell to Bedside
Philadelphia: WB Saunders, Co., 1990; 291–9.
[24] Marron K, Wharton J, Sheppard MN, et al. Distribution,
morphology, and neurochemistry of endocardial and epicardial nerve terminal arborizations in the human heart.
Circulation 1995; 92: 2343–51.
[25] Waxman MB, Cameron DA, Wald RW. Role of ventricular
vagal afferents in the vasovagal reaction (editorial). J Am Coll
Cardiol 1993; 21: 1138–41.
[26] Warner HR, Cox A. A mathematical model of heart rate
control by sympathetic and vagus efferent information. J Appl
Physiol 1962; 17: 349–55.
[27] van Lieshout JJ, Wieling W, Karemaker JM, Eckberg DL.
The vasovagal response. Clin Sci 1991; 81: 575–86.
[28] Wahbha MM, Morley CA, al Shamma YM, Hainsworth R.
Cardiovascular reflex responses in patients with unexplained
syncope. Clin Sci 1989; 77: 547–53.
[29] Abboud FM. Neurocardiogenic syncope (editorial). N Engl J
Med 1993; 328: 1117–20.
[30] Rea RF. Neurally mediated hypotension and bradycardia:
Which nerves? How mediated? (editorial). J Am Coll Cardiol
1989; 14: 1633–4.
[31] Rea RF, Thames MD. Neural control mechanisms and vasovagal syncope. J Cardiovasc Electrophysiol 1993; 4: 587–95.
[32] Milstein S, Buetikofer J, Lesser J, et al. Cardiac asystole: a
manifestation of neurally mediated hypotension-bradycardia.
J Am Coll Cardiol 1989; 14: 1626–32.
[33] Benditt DG, Erickson M, Gammage MD, Markowitz T,
Sutton R. A synopsis: neurocardiogenic syncope, an international symposium, 1996. Pacing Clin Electrophysiol 1997;
20: 851–60.
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