1216

Reentrant Ventricular Tachycardia Originating from the AorticSinus Cusp: A Case Report

TAKESHI TSUCHIYA, M.D., KUNIHIKO YAMAMOTO, M.D.,∗ ERIKO TANAKA, M.D.,∗

and HIDEKI TASHIRO, M.D.∗

From the Division of Cardiology, Hakuaikai Hospital, Kumamoto, Japan; and∗Division of Cardiology, St. Mary Hospital, Kurume, Japan

Reentrant VT from Aortic Sinus Cusp. We report a case of idiopathic reentrant ventricular tachy-cardia (VT) originating from the left aortic sinus cusp. A prepotential preceding the QRS complex by 58 mswas recorded from the posterior right ventricular (RV) outflow tract. During VT entrainment observed bypacing from the midseptal RV, it initially was orthodromically captured with a long conduction time but thenantidromically captured as the pacing cycle rate was increased. Pacing at that site failed to show concealedentrainment despite a postpacing interval similar to the VT cycle length. Radiofrequency catheter ablationabolished the VT in the left aortic sinus cusp where a prepotential preceding the QRS complex by 78 mswith a postpacing interval similar to the VT cycle length was recorded in addition to concealed entrainment.The findings suggest that, in this VT, a critical slow conduction zone is partially present extending from theleft aortic sinus cusp to the posterior right ventricular outflow tract. The patient has remained free fromVT recurrence after 5-month follow-up. (J Cardiovasc Electrophysiol, Vol. 15, pp. 1216-1219, October 2004)

aortic sinus cusp, entrainment, radiofrequency catheter ablation, reentrant ventricular tachycardia

Introduction

Idiopathic ventricular tachycardia (VT) originating fromthe aortic sinus cusp can be encountered in the clinical set-ting.1-4 The VT can be abolished by radiofrequency (RF)catheter ablation, and the mechanism is nonreentrant in mostcases.1-3 A few isolated reports have described a reentrant VToriginating from the aortic sinus cusp.4 We report a case of id-iopathic reentrant VT originating from the aortic sinus cusp.The anatomic location of the slow conduction zone and elec-trophysiologic characteristics of the slow conduction zonewere examined using an entrainment technique.

Case ReportA 37-year-old woman was admitted to our hospital for treat-

ment of symptomatic VT that was frequent and refractory toantiarrhythmic agents. ECG recorded during the VT showeda left bundle branch block pattern in the precordial leads andan inferior axis. This pattern fulfilled the criteria of VT orig-inating from the aortic sinus cusp reported by Ouyang et al.2

(Fig. 1). ECG recorded during sinus rhythm showed a normalQRS morphology and ST-T segment. Extensive investigation in-cluding echocardiography, left and right ventriculography, andcoronary angiography revealed no structural heart disease.

Informed written consent was obtained from the patient.Electrophysiologic study was performed using the standardtechnique, with no antiarrhythmic agents and the patient ina fasting state. Sustained VT with a cycle length of 325 msecand the same QRS morphology as the clinical arrhythmia wasrepeatedly induced by a single extrastimulus from the right ven-tricular (RV) apex.

During rapid pacing from the midseptal RV during the VT,classic entrainment criteria, including constant fusion and pro-

Address for correspondence: Takeshi Tsuchiya, M.D., Division of Cardi-ology, Hakuaikai Hospital, 4-3, Konya-ima machi, 860-0012 Japan. Fax:81-96-326-5974; E-mail: tsuchiya@s1.kcn-tv.ne.jp

Manuscript received 19 December 2003; Revised Manuscript received29 February 2004; Accepted for publication 4 April 2004.

doi: 10.1046/j.1540-8167.2004.03695.x

gressive fusion, were fulfilled, suggesting that the mechanismof VT was reentry with an excitable gap (Fig. 2). Double po-tentials preceding the QRS complex by 58 ms were recordedfrom the posterior RV outflow tract (RVOT). The first compo-nent of the double potentials (indicated by “x” in Fig. 2) wascaptured orthodromically by pacing from the midseptal RVat a pacing rate of 225 beats/min because the morphology ofthe first component during pacing was the same as that dur-ing the spontaneous VT, and the time interval between the lastelectrogram activated by the pacing stimulus to the initial elec-trogram of the spontaneous VT after pacing was equal to thepacing cycle length. In contrast, the morphology of the secondcomponent of the double potentials (indicated by “y” in Fig. 2)

Figure 1. ECG recorded during ventricular tachycardia.

Tsuchiya et al. Reentrant VT from Aortic Sinus Cusp 1217

Figure 2. Constant and progressive fusion observed during VT entrainment by pacing from the mid right ventricular septum. Left panel: VT entrainmentat a pacing rate of 225 beats/min. Right panel: VT entrainment at a pacing rate of 245 beats/min. Recordings from ECG leads I, aVF, and V1 and bipolarelectrograms recorded from the His-bundle region (His), distal and proximal posterior right ventricular outflow tract (RVOTd and RVOTp), and distal toproximal sites of the coronary sinus (CS) are shown. A prepotential, the first component of the double potentials, was recorded from the posterior RVOT(arrows). “x” and “y” indicate the first and second components of the double potentials recorded at the posterior RVOT, respectively. Numbers indicatethe time intervals, and numbers in circles indicate conduction time. Numbers are in milliseconds. The time interval from the last pacing stimulus artifact tothe first component of the initial spontaneous VT beat at a pacing rate of 225 beats/min was 295 ms, whereas the conduction time from the pacing stimulusartifact to the ventricular electrogram at the proximal coronary sinus was 100 ms.

Figure 3. Activation and entrainment mapping of the VT. A: A mapping catheter was positioned at the left aortic sinus cusp (ASC). A discrete prepotentialwas recorded from the ASC and is expressed as a small negative deflection (arrows) in the unipolar recording. B: Concealed entrainment observed duringpacing from the left ASC. In each panel, the tracings are from ECG leads I, (aVR, aVL), aVF, and V1, bipolar electrograms recorded from serial sites ofthe right ventricular outflow tract, and bipolar and unipolar electrograms recorded from the ASC. Numbers indicate the time intervals (in milliseconds).Concealed entrainment was observed by pacing from the ASC with a postpacing interval similar to the VT cycle length.

1218 Journal of Cardiovascular Electrophysiology Vol. 15, No. 10, October 2004

Figure 4. Elimination of VT by radiofrequency catheter ablation (RFCA) delivered to the left aortic sinus cusp. The VT terminated 4.5 seconds after initiationof RFCA. Tracings as in Figure 3. B: Location of the electrode catheters in RAO and LAO views during left coronary arteriography. ABL = ablation catheter;CS = coronary sinus; His = His-bundle region; RVOT = right ventricular outflow tract.

during pacing was different from that during the spontaneousVT, indicating antidromic capture. When a detailed analysis ofthe conduction time was performed during VT entrainment,a slow conduction zone was detected between the midseptalRV and posterior RV, because the posterior RV was ortho-dromically captured by pacing from the midseptal RV witha long conduction time. On the other hand, the area betweenthe mid-RV and distal coronary sinus was considered to bethe non–slow conduction area because the distal coronary sinuswas captured antidromically with a relatively short conductiontime.5

When the pacing rate was increased to 245 beats/min, themorphology of the first component was different between pacingand spontaneous VT. The sequence of the first and second com-ponents were reversed during pacing, and the time differencebetween the last electrogram activated by the pacing stimulusto the initial electrogram of the spontaneous VT after pacingdid not equal the pacing cycle length, suggesting antidromiccapture of the first component. With rapid pacing from the pos-terior RVOT during VT, the time difference between the pacingstimulus artifact and the electrogram was 18 ms; however, con-cealed entrainment was not observed in the QRS complex. Thesefindings suggest that the posterior RVOT is the exit site of thereentrant circuit.6

We performed detailed activation mapping in the aortic si-nus cusp because it is located just posterior to the posteriorRVOT. A discrete prepotential exhibiting a QS pattern in the

unipolar recordings preceded the QRS complex by 78 ms at theleft aortic sinus cusp (Fig. 3, left panel). With rapid pacing fromthat site during VT, concealed entrainment in the QRS complexwas observed, as was a similar time difference between the pac-ing stimulus artifact and the first electrogram at the site afterpacing (Fig. 3, right panel). The findings suggest that the siteis in the critical slow conduction zone.6 Together with the ear-lier observations, the findings suggest that the excitation thatpropagated through the slow conduction zone, which includedthe left aortic sinus cusp, broke away toward the posteriorRVOT.

The site was located about 1.0 cm anteroinferior to the leftcoronary artery ostium in the left aortic sinus cusp, which wasobserved during coronary angiography performed while theelectrode catheter was placed at the site (Fig. 4, right panel).Delivery of 20-W RF energy to the site resulted in VT ter-mination 4.5 seconds after initiation of RF energy application(Fig. 4, left panel). Subsequently, the VT was no longer inducibleby RV extrastimuli or burst pacing before or after isoproterenoladministration (1 µg/min). After successful ablation, a delayedpotential was recorded during sinus rhythm at the successfulablation site (data not shown).

Echocardiography performed after RF ablation showed noaortic valve abnormalities or any aortic regurgitation flow pat-terns by Doppler echocardiography. The patient has remainedfree from VT recurrence with no antiarrhythmic agents after5-month follow-up.

Tsuchiya et al. Reentrant VT from Aortic Sinus Cusp 1219

Discussion

This case illustrates a VT originating from the aortic si-nus cusp and involving the myocardium on the aortic cuspsand RVOT. Entrainment mapping suggested reentry as theunderlying mechanism. With detailed analysis of the con-duction time during the VT entrainment, a critical slowconduction zone was considered to be partially present,extending from the left aortic sinus cusp to the posteriorRVOT.

Li et al.4 described a reentrant VT originating from theaortic sinus cusp, in which an inverse relationship betweenthe last coupling interval of the programmed ventricular stim-ulation and the interval from the last stimulus to the first beatof the induced VT was observed. In the present case, the VTmechanism was shown to be reentry with an excitable gap,given observation of entrainment criteria including constantfusion, progressive fusion, and electrogram change equiva-lent to progressive fusion.

Ouyang et al.2 reported that a low-amplitude, high-frequency potential preceding the local ventricular potentialwas always found at the aortic sinus cusp during the VT in pa-tients with an aortic sinus cusp origin of repetitive monomor-phic VT. That the potential presented as a presystolic activa-tion during the VT but was the second ventricular activationcomponent during sinus rhythm suggests a slow conductionarea between the ventricle and the aortic sinus cusp. Althoughthe VT in this patient was not a repetitive monomorphic VTbut a reentrant VT, a similar low-amplitude, high-frequencypotential was observed during the VT and sinus rhythm atthe aortic sinus cusp. Together with the observations duringVT entrainment, the findings suggest that a connection be-tween the ventricle and the aortic sinus cusp acts as a slowconduction zone.

With regard to anatomy, Ya et al.7 reported that during em-bryogenesis in animal hearts, the distal portion of the outflowtract loses its myocardial phenotype and becomes the prox-imal portion of the ascending aorta and pulmonary trunk.A muscular connection suggested to be present between theaortic sinus cusp and the RVOT may have served as the slowconduction zone in the present patient.

Acknowledgments: The authors thank Mr. Katsunori Yamashita and Mr.Tomohisa Inoue for technical assistance.

References

1. Kanagaratnam L, Tomassoni G, Schweikert R, Pavia S, Bash D,Beheiry S, Niebauer M, Saliba W, Chung M, Tchou P, Natale A: Ven-tricular tachycardia arising from the aortic sinus of Valsalva: An under-recognized variant of left outflow tract ventricular tachycardia. J AmColl Cardiol 2001;37:1408-1414.

2. Ouyang F, Fotuhi P, Volkmer M, Goya M, Burns M, Ant M, Ernst S,Cappato R, Kuck KH: Repetitive monomorphic ventricular tachycardiaoriginating from the aortic sinus cusp: Electrocardiographic character-ization for guiding catheter ablation. J Am Coll Cardiol 2002;39:500-508.

3. Hachiya H, Aonuma K, Yamauchi Y, Igawa M, Nogami A, Iesaka Y:How to diagnose, locate, and ablate coronary cusp ventricular tachycar-dia. J Cardiovasc Electrophysiol 2002;13:551-556.

4. Li YG, Gronefeld G, Israel C, Hohnloser SH: Sustained monomorphicventricular tachycardia ablation from the aortic sinus of Valsalva. J Car-diovasc Electrophysiol 2002;13:130-134.

5. Tsuchiya T, Okumura K, Honda T, et al: Significance of late diastolicpotential preceding Purkinje potential in verapamil-sensitive idiopathicleft ventricular tachycardia. Circulation 1999;99:2408-2413.

6. Stevenson WG: Catheter mapping and ablation of ventricular tachycar-dia later after myocardial infarction. In Huang SKS, ed: RadiofrequencyCatheter Ablation of Cardiac Arrhythmias. Armonk, NY: Futura Pub-lishing Co., 1995:491-519.

7. Ya J, van den Hoff MJB, de Boer PAJ, Tesink-Taekema S, Franco D,Moorman AFM, Lamers WH: Normal development of the outflow tractin the rat. Circ Res 1998;82:464-472.