CASE REPORT

Vagal reflex provoked by radiofrequency catheterablation in the right aortic sinus cusp:a Bezold–Jarisch-like phenomenon

Takumi Yamada & Yukihiko Yoshida & Yasuya Inden &

Toyoaki Murohara & G. Neal Kay

Received: 9 February 2008 /Accepted: 24 June 2008 /Published online: 30 August 2008# Springer Science + Business Media, LLC 2008

Abstract A 66-year-old woman with idiopathic prematureventricular contractions with a left bundle branch blockQRS morphology and left inferior axis underwent electro-physiologic testing. Successful radiofrequency ablation wasachieved in the right coronary cusp (RCC). However,radiofrequency ablation at sites adjacent to the successfulablation site provoked sinus bradycardia followed byatrioventricular conduction block. That phenomenon mightbe explained by a vagal reflex through stimulation of vagalpathways or receptors in the anterior epicardial fat padsneighboring to the RCC. A vagal reflex should be kept inmind as a complication during catheter ablation ofventricular arrhythmias originating from the RCC.

Keywords Vagal reflex . Premature ventricular contraction .

Right aortic sinus cusp . Radiofrequency catheter ablation

1 Introduction

Aortic sinus cusps (ASCs) are known to be one of themajor sources of idiopathic ventricular tachycardia orpremature ventricular contractions (PVCs) [1–4]. Thoughit has been reported that radiofrequency (RF) catheterablation can be safely performed in the ASCs [1–4], theanatomical specificity of the ASCs may be expected toresult in serious complications associated with the coronaryarteries and aortic valve. We report a case with anunexpected complication during the RF catheter ablationin the right aortic sinus cusp (RCC).

2 Case report

A 66-year-old woman with symptomatic idiopathic PVCsunderwent electrophysiologic testing. Echocardiographyand an exercise stress test demonstrated no evidence ofstructural heart disease. Written informed consent wasobtained, and all antiarrhythmic drugs were discontinuedfor more than at least five half-lives prior to the study. Anelectrophysiologic study was undertaken in the fastingstate. She was given intravenous sedation with pentazocineand midazolam. At baseline, the cycle length of sinusrhythm was 800ms and bigeminal or trigeminal PVCspersisted. The PVCs had a left bundle branch block and leftinferior axis QRS morphology and a QRS transitionbetween V2 and V3 (Fig. 1). First, a 7-French, 4-mm tipablation catheter was introduced into the right ventricularoutflow tract (RVOT) via the right femoral vein formapping. During PVCs, the earliest ventricular activation

J Interv Card Electrophysiol (2008) 23:199–204DOI 10.1007/s10840-008-9292-4

T. Yamada (*) :G. N. KayDivision of Cardiovascular Disease,University of Alabama at Birmingham,VH, B147, 1670 University Boulevard, 1530 3rd AVE S,Birmingham, AL 35294-0019, USAe-mail: takumi-y@fb4.so-net.ne.jp

Y. YoshidaDivision of Cardiology, Cardiovascular Center,Nagoya Dai-ni Red Cross Hospital,Nagoya, Japan

Y. Inden : T. MuroharaDepartment of Cardiology,Nagoya University Graduate School of Medicine,Nagoya, Japan

in the RVOT preceded the QRS onset by about 20ms, but apace map at that site was not excellent. Next, a 7-French,decapolar catheter with a lumen was introduced into thecoronary sinus (CS) via the right subclavian vein and a 2.3-French multielectrode catheter was introduced into the greatcardiac vein through the CS catheter. During PVCs, theearliest ventricular activation in the great cardiac vein waslater than that in the RVOT (Fig. 1). Following that, another7-French, 4-mm tip ablation catheter was introduced intothe ASCs via the right femoral artery for mapping. Duringthe mapping of the ASCs, intravenous heparin wasadministered to maintain an activated clotting time >250s.Selective angiography of the coronary arteries and aortawas performed to assess the anatomic relationships betweenthe ASCs and the location of the ablation catheter. DuringPVCs, the earliest ventricular activation preceding the QRSonset by 54ms was observed in the RCC, where a pace mapwas almost perfect and no His bundle (HB) electrogramwas recorded (Figs. 1 and 2). An RF application with atarget temperature of 55°C and maximum power output of30W was then delivered at that site, resulting in the

suppression of the PVCs. However, during the RFapplication, the cycle length of sinus rhythm graduallyprolonged up to 900ms and then greatly prolonged (themaximal cycle length = 1,200ms) 25s after the RFapplication was started, and the RF energy delivery wasimmediately stopped (Fig. 1). The patient reported no chestsymptoms during that RF application. Because soon afterthat, sinus rate recovered to the baseline level, the RFapplication was delivered at the same site again. However,the same phenomenon occurred and the session was ended.Selective angiography of the coronary arteries showed nosignificant abnormalities.

The PVCs recurred soon after the first session, and asecond session was performed 2 months after the firstprocedure. At baseline, the cycle length of sinus rhythmwas 920ms and bigeminal or trigeminal PVCs persisted.The PVCs had almost the same QRS morphology as in thefirst session (Fig. 3). Multipolar catheters were introducedinto the high right atrium and HB region via the rightfemoral vein for mapping and pacing. A 7-French, 4-mmtip ablation catheter was introduced into the RCC via the

Fig. 1 Twelve-lead electrocardiograms during a premature ventricularcontraction (PVC) and pace mapping at the ablation site in the rightcoronary sinus cusp (RCC; left panel), cardiac tracings showing theablation site (mid panel) and sinus bradycardia occurring during the

radiofrequency (RF) ablation (right panel). ABL(RVOT)d,p the distaland proximal electrode pairs of the ablation (right ventricular outflowtract) catheter, CSd,p the electrode pairs of the distal and proximalcoronary sinus catheters, PM pace map

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right femoral artery for mapping. During the mapping ofthe ASCs, intravenous heparin was administered to main-tain an activated clotting time >250s. Selective angiographyof the right coronary artery showed no significant abnor-malities (Fig. 2). During PVCs, a pre-potential precedingthe QRS onset by 44ms was observed at the earliestventricular activation site in the RCC, where a pace mapwas not excellent and no HB electrogram was recorded(Figs. 2 and 3). An RF application with a target temperatureof 55°C and maximum power output of 30W was thendelivered at that site, and 3s after the RF application started,the PVCs were eliminated without any occurrence ofbradycardia (Fig. 3). Following that, an insurance burnwith the same RF ablation settings was delivered slightlyon the antero-superior side of the successful ablation site,where no HB electrogram was recorded (Fig. 4). During theRF application, the cycle length of sinus rhythm graduallyprolonged up to 1,500ms and then atrioventricular conduc-tion block suddenly occurred (the longest pause = 2.8s) 13safter the RF application was started, and the RF energydelivery was immediately stopped and back up pacing fromthe right ventricle was delivered (Fig. 4). The patientreported no chest symptoms during that RF application.

The sinus rate and atrioventricular conduction recovered tothe baseline level soon after that. Selective angiography ofthe coronary arteries revealed no significant abnormalities.During more than one year of follow-up, this patient hasbeen free of any symptomatic PVCs or bradycardia withoutany antiarrhythmic drugs.

3 Discussion

Serious complications such as a chronic left main coronaryartery occlusion [5] or aortic regurgitation may be expectedto occur in the catheter ablation of ventricular tachycardiasor PVCs originating from the ASCs. However, thosecomplications may be prevented if the RF ablation isperformed while an angiographic catheter is deployed in theostium of the coronary artery with frequent manual contrastinjections when the ablation site is close to the ostium of acoronary artery, or if no high RF energy is delivered with atemperature control. A vagal reflex might be evoked byphysical and/or mental stress during a long-standingelectrophysiologic study or chest pain may be caused by

Fig. 2 Right coronary arteryangiograms (RCAG) and theablation sites in the RCC. Theablation catheter is located atthe successful ablation site. Theopen star indicates the ablationsite in the first session andthe solid star the site of theinsurance burn in the secondsession. HB His bundle catheter,HRA high right atrium, LAO theleft anterior oblique view, RAOthe right anterior oblique view.The other abbreviations are as inFig. 1

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an RF energy delivery. Such secondary reasons seemedvery unlikely in this case. A vagal reflex has been reportedas a complication during the catheter ablation of leftaccessory pathways [6, 7] and atrial fibrillation [8, 9].However, to the best of our knowledge, this is the firstreport describing a vagal reflex as a complication during thecatheter ablation of ventricular arrhythmias originatingfrom the ASCs. In the previous reports [6–9], the proposedcausal mechanism was explained by a reflexogenicallymediated hypotension-bradycardia syndrome (Bezold–Jar-isch-like phenomenon) through stimulation of either nearbyvagal afferent pathways or sensory terminal receptors at theablation site. The human epicardial fat pads (FPs) containvagal pathways and parasympathetic ganglia [10–13]. Inthe previous cases [6–9], the FPs located at the junction ofthe inferior vena cava and inferior left atrium and at thepulmonary vein-left atrium might be associated with thevagal reflex. In the aorto-pulmonary window in humans,there is an anterior epicardial FP containing parasympa-thetic ganglia [14]. Cummings et al. have demonstrated bydirect stimulation of the human anterior epicardial FP at the

time of coronary artery bypass surgery that the anteriorepicardial FP provides parasympathetic innervation to thesino-atrial node [14]. Anatomical studies have demonstrat-ed that the anteriorly situated right ventricular outflow tractpasses slightly superior to and leftward of the aortic valve[2, 15]. Though the RCC is adjacent to the pulmonaryinfundibulum, there is a cleavage plane behind thepulmonary infundibulum and in front of the aortic root[2]. The space between the pulmonary infundibulum andRCC should be filled with the anterior epicardial FP.Therefore, RF energy delivery from the RCC may give athermal effect to the anterior epicardial FP, resulting in avagal stimulation. A vagal reflex should be kept in mind asa complication in the catheter ablation of ventriculararrhythmias originating from the RCC.

Because anatomically, the ganglionated plexuses areembedded in the paraaortic fat pad adjacent to the leftcoronary cusp as well as the RCC [16], a greater incidenceof such a complication may be expected. However, theparaaortic fat pad is usually located above the level of thecoronary artery ostium which is located above the myocar-

Fig. 3 Twelve-lead electrocardiograms during a PVC in the secondsession and pace mapping at the successful ablation site in the RCC(left panel), cardiac tracings showing the successful ablation site (midpanel) and successful ablation (right panel). The arrowhead indicates

the pre-potential recorded at the successful ablation site. HBd,m,p thedistal, middle and proximal electrode pairs of the His bundle catheter.The other abbreviations are as in the previous figures

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dium of the aortic root as a target for catheter ablation.Therefore, such a complication may occur in only rarecases with some anatomical variants. In this case, the rightcoronary artery ostium was located very posteriorly,contiguous to the non-coronary cusp and at a lower levelof the RCC than usual (Fig. 2). Consequently, the RFablation sites on the anterior myocardium of the aortic rootwere located above the right coronary artery ostium(Fig. 2). Those anatomical considerations may explain theoccurrence of that rare complication in this case.

Acknowledgement There was no financial support for this study.

References

1. Kanagaratnam, L., Tomassoni, G., Schweikert, R., Pavia, S.,Bash, D., Beheiry, S., et al. (2001). Ventricular tachycardiasarising from the aortic sinus of valsalva: an under-recognizedvariant of left outflow tract ventricular tachycardia. Journal of theAmerican College of Cardiology, 37, 1408–1414.

2. Ouyang, F., Fotuhi, P., Ho, S. Y., Hebe, J., Volkmer, M., Goya,M., et al. (2002). Repetitive monomorphic ventricular tachycardiaoriginating from the aortic sinus cusp: electrocardiographic

characterization for guiding catheter ablation. Journal of theAmerican College of Cardiology, 39, 500–508.

3. Ito, S., Tada, H., Naito, S., Kurosaki, K., Ueda, M., Hoshizaki, H., etal. (2003). Development and validation of an ECG algorithm foridentifying the optimal ablation site for idiopathic ventricular outflowtract tachycardia. Journal of Cardiovascular Electrophysiology, 14,1280–1286.

4. Hachiya, H., Aonuma, K., Yamauchi, Y., Igawa, M., Nogami, A.,& Iesaka, Y. (2002). How to diagnose, locate, and ablate coronarycusp ventricular tachycardia. Journal of Cardiovascular Electro-physiology, 13, 551–556.

5. Pons, M., Beck, L., Leclercq, F., Ferriere, M., Albat, B., & Davy,J. M. (1997). Chronic left main coronary artery occlusion: acomplication of radiofrequency ablation of idiopathic left ventric-ular tachycardia. Pacing and Clinical Electrophysiology, 20,1874–1876.

6. Schlapfer, J., Kappenberger, L., & Fromer, M. (1996). Bezold–Jarisch-like phenomenon induced by radiofrequency ablation of aleft posteroseptal accessory pathway via the coronary sinus.Journal of Cardiovascular Electrophysiology, 7, 445–449.

7. Tsai, C. F., Chen, S. A., Chiang, C. E., Tai, C. T., Lee, S. H., Wen,Z. C., et al. (1997). Radiofrequency ablation-induced asystoleduring transaortic approach for a left anterolateral accessorypathway: a Bezold–Jarisch-like phenomenon. Journal of Cardio-vascular Electrophysiology, 8, 694–699.

8. Tsai, C. F., Chen, S. A., Tai, C. T., Chiou, C. W., Prakash, V. S.,Yu, W. C., et al. (1999). Bezold–Jarisch-like reflex duringradiofrequency ablation of the pulmonary vein tissues in patientswith paroxysmal focal atrial fibrillation. Journal of CardiovascularElectrophysiology, 10, 27–35.

Fig. 4 Cardiac tracings showing the site of the insurance burn (left panel) and sinus bradycardia followed by atrioventricular conduction blockoccurring during the RF ablation (right panel). The abbreviations are as in the previous figures

J Interv Card Electrophysiol (2008) 23:199–204 203203

9. Pappone, C., Santinelli, V., Manguso, F., Vicedomini, G.,Gugliotta, F., Augello, G., et al. (2004). Pulmonary veindenervation enhances long-term benefit after circumferentialablation for paroxysmal atrial fibrillation. Circulation, 109, 327–334.

10. Singh, S., Johnson, P. I., Lee, R. E., Orfei, E., Lonchyna, V. A.,Sullivan, H. J., et al. (1996). Topography of cardiac ganglia in theadult human heart. The Journal of Thoracic and CardiovascularSurgery, 112, 943–953.

11. Quan, K. J., Lee, J. H., Geha, A. S., Biblo, L. A., Van Hare, G. F.,Mackall, J. A., et al. (1999). Characterization of sinoatrialparasympathetic innervation in humans. Journal of CardiovascularElectrophysiology, 10, 1060–1065.

12. Quan, K. J., Lee, J. H., Van Hare, G. F., Biblo, L. A., Mackall, J.A., & Carlson, M. D. (2001). Identification and characterization of

atrioventricular parasympathetic innervation in humans. Journalof Cardiovascular Electrophysiology, 13, 735–739.

13. Carlson,M.D., Geha, A. S., Hsu, J., Martin, P. J., Levy,M. N., Jacobs,G., et al. (1992). Selective stimulation of parasympathetic nerve fibersto the human sinoatrial node. Circulation, 85, 1311–1317.

14. Cummings, J. E., Gill, I., Akhrass, R., Dery, M., Biblo, L. A., &Quan, K. J. (2004). Preservation of the anterior fat padparadoxically decreases the incidence of postoperative atrialfibrillation in humans. Journal of the American College ofCardiology, 43, 994–1000.

15. Anderson, R. H. (2000). Clinical anatomy of the aortic root. Heart(British Cardiac Society), 84, 670–673.

16. Armour, J. A.,Murphy, D. A., Yuan, B. X.,Macdonald, S., &Hopkins,D. A. (1997). Gross and microscopic anatomy of the human intrinsiccardiac nervous system. The Anatomical Record, 247, 289–298.

204 J Interv Card Electrophysiol (2008) 23:199–204