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Journal of Electrocardiology 45 (2012) 170–175www.jecgonline.com

Electrocardiographic, electrophysiologic, and anatomical features ofventricular tachycardia originating from noncoronary cusp☆

Sima Sayah, MD, Shahab Shahrzad, MD, Mehdi Moradi, MD,Majid Haghjoo, MD, FACC, FESC⁎

Cardiac Electrophysiology Research Center, Rajaie Cardiovascular Medical and Research Center, Tehran University of Medical Sciences, Tehran, Iran

Received 17 August 2011

Abstract In this article, we report 2 young patients (a 15-year-old adolescent girl and a 25-year-old man) with

☆ Conflict of inte⁎ Corresponding

Rajaie CardiovascularMellat Park, Vali-E-A

E-mail addresses:

0022-0736/$ – see frodoi:10.1016/j.jelectroc

drug-refractory palpitations. Admission electrocardiograms showed runs of ventricular tachycardiawith left bundle-branch block morphology, left inferior axis, early precordial QRS transition, andpositive QRS complex in lead I. In right ventricular mapping, the earliest activation site was found inthe His bundle region. Aortic root mapping showed a very early fractionated ventricular signal withlarge atrial potential and no His potential in the noncoronary cusp region. Radiofrequency energyapplication in this region resulted in tachycardia termination within 5 to 10 seconds. During a 3- to 6-month follow-up period, the patients remained asymptomatic, and the electrocardiogram showed noventricular arrhythmias.© 2012 Elsevier Inc. All rights reserved.

Keywords: Ventricular tachycardia; Noncoronary cusp; Ablation

Case presentation

Case 1

A 15-year-old adolescent girl presented to the emergencydepartment because of sudden onset palpitations. Theproblem had commenced 2 weeks before admission, andduring this period, she had experienced frequent episodes ofpalpitations, which were refractory to the twice dailyadministration of 80 mg of sotalol. The patient had nothingsignificant in her history, and there was no history of similarproblem in other family members.

On admission, the patient had a blood pressure of 115/70mm Hg and pulse rate of 158 beats per minute, and she feltpalpitation without any dizziness. In cardiac auscultation,she had variable S1 with normal S2 without any murmur.The rest of the physical examination result was normal. Theadmission electrocardiogram (ECG) showed repetitive non-sustained wide QRS tachycardia with left bundle-branchblock (LBBB) morphology, left inferior axis, positive QRScomplexes in leads I and aVL, QS morphology in aVR, QRStransition between V2 and V3, and absence of S wave in lead

rest: None to declare.author. Cardiac Electrophysiology Research Center,Medical and Research Center, P.O. Box: 15745-1341,sr Avenue, Tehran 1996911151 Iran.majid.haghjoo@gmail.com, haghjoo@rhc.ac.ir

nt matter © 2012 Elsevier Inc. All rights reserved.ard.2011.10.009

V6 (Fig. 1A). Details of the ECG characteristics aredescribed in the Table 1. Transthoracic echocardiographyshowed normal right and left ventricular functions.

Considering the drug-refractory palpitations, the patientwas scheduled for electrophysiology (EP) study andablation. After providing the patient with detailed descriptionof the EP study and the catheter ablation, written informedconsent was obtained. Antiarrhythmic medication waswithdrawn for at least 5 half-lives before the procedure.Three quadripolar 7F catheters were placed in the high rightatrium, right ventricular (RV) apex, and His bundle region.During the study, tachycardia started spontaneously: it was aregular wide QRS tachycardia (cycle length, 380 ms) withcomplete AV dissociation and negative HV interval in favorof ventricular tachycardia (VT). QRS morphology and axiswere identical to clinical tachycardia. Given the ECGcharacteristics of the VT, a steerable 4-mm ablation catheterwas initially advanced to the RV outflow tract (RVOT) fordetailed activation mapping. The earliest activation site(preceding the QRS onset by 44 ms) was found in the Hisbundle region. With respect to the anatomical proximity andthe lower risk of atrioventricular block, it was decided to mapthe right coronary (RCC) and noncoronary (NCC) aorticcusps. Before catheter mapping, aortography showednormally functioning 3-cusp aortic valve and patent coronaryarteries. Aortic root mapping showed a very early signal (74ms earlier than QRS onset) with large atrial potential, and

Fig. 1. Twelve-lead ECG recorded in 2 cases during VT. A, There is VT with LBBBmorphology, left inferior axis, QRS transition between V2 and V3, R wave inlead I, RR' in aVL, and absence of S wave in lead V6. B, This ECG similarly shows nonsustained VT with LBBB morphology, left inferior axis, QRS transitionat V3, RR' in lead I, and absence of S wave in lead V5 through V6. However, there is QS complex in aVL, and QRS duration is slightly wider (180 vs 132 ms).

171S. Sayah et al. / Journal of Electrocardiology 45 (2012) 170–175

small fractionated ventricular potential in the NCC region(Fig. 2A). Pacing at the NCC captured the atrium but not theventricle (Fig. 3). Single radiofrequency energy application(30 W, 50°C) at the earliest activation site in the NCCresulted in VT termination within 10 seconds. At thesuccessful site, the fluoroscopic location of the ablationcatheter was very close to the His catheter (Fig. 2B, C).Subsequent programed ventricular stimulation with andwithout isoproterenol failed to induce any ventriculararrhythmias. Predischarge clinical examination, ECG, andtransthoracic echocardiography revealed no abnormality.During a 7-month follow-up period, the patient remainedasymptomatic, and her ECG showed no VT or premature

ventricular complex (PVC). There was no evidence ofventricular arrhythmias in 24-hour ECG monitoring per-formed 1 month after ablation.

Case 2

A 25-year-old man presented with drug-refractorypalpitations and dyspnea on exertion. He had a history ofpreviously failed ablation in the RVOT. During theprevious 10 months, he had experienced a significantdecrease in the left ventricular ejection fraction (LVEF). Onadmission, physical examination was unremarkable. TheECG showed runs of wide QRS tachycardia with LBBB

Fig. 2. Local EGM and catheter positions at the successful ablation site in case 1. A, First beat is sinus, and second and third beats are first 2 beats of VT. Hispotential is clearly recorded in sinus beat. Both sinus and VT beat show a large atrial potential and a small multicomponent ventricular potential. During VT,fractionated ventricular potential recorded in the ablation catheter preceded the QRS onset by 74 ms. B and C, Note that the ablation catheter is located near theHis catheter both in right anterior and left anterior oblique views. aVF, V1, and V5 indicate surface ECG leads; HRA-D, the distal electrode pair of the catheterplaced in high right atrium; HIS-D, the distal electrode pair of the catheter placed in RV His bundle region; ABL-D, the distal electrode pair of the ablationcatheter; ABL Uni, the distal unipolar electrode of the ablation catheter; HRA, catheter at high right atrium; HIS, His bundle catheter; RVA, RV catheter at apex;ABL, ablation catheter.

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morphology, left inferior axis, notched R wave in lead I,QS complex in lead aVL, QS morphology in aVR, QRStransition at V3, and absence of S wave in lead V6

(Fig. 1B). The ECG features are depicted in more detail inTable 1. Transthoracic echocardiography showed depressedleft ventricular (LV) function (LVEF, 30%) and dilated LVand RV dimensions.

Considering the drug-refractory palpitations and de-creased LV function, the patient was scheduled for EPstudy and ablation. Detailed mapping of the RVOT showedthe earliest ventricular activation near the His bundle region(16 ms earlier than QRS onset). Decision was, therefore,made to map the RCC and NCC. Mapping of the NCCrevealed an early signal (preceded the QRS onset by 52 ms)

Fig. 3. Pacing from NCC. Note that pacing from this region captured the atrium. aVF, V1, and V5 indicate surface ECG leads; HRA-D, the distal electrode pair ofthe catheter placed in high right atrium; HIS-D, the distal electrode pair of the catheter placed in RV His bundle region; ABL-D, the distal electrode pair of theablation catheter; ABL Uni, the distal unipolar electrode of the ablation catheter.

Table 1ECG characteristics of patients during VT

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with large atrial potential and small fractionated ventricularpotential (Fig. 4A). Pacing via catheter ablation captured theatrium. Aortography confirmed the location of the catheterwithin the NCC and showed tricuspid normally functioningaortic valve and patent coronary arteries (Fig. 4B, C).Radiofrequency energy delivery (30W, 50°C) at this locationresulted in VT termination within 5 seconds, and notachycardia was inducible with and without isoproterenol.Predischarge examination and ECG showed no abnormality,and echocardiography showed slightly improved LV func-tion (LVEF, 35%). During a 3-month follow-up period, thepatient had no palpitations, and ECG showed no ventriculararrhythmias. One month after ablation, ambulatory ECGmonitoring showed no PVC or VT, and echocardiographyrevealed dramatically improved LV function (LVEF, 50%).

ECG characteristic Case 1 Case 2

Total QRS duration (ms) 132 180R-wave duration in lead V1 (ms) 34 34R-wave duration in lead V2 (ms) 60 62R-/S-wave amplitude ratio in lead V1 (%) 5 15R-/S-wave amplitude ratio in lead V2 (%) 20 14R-wave duration index in lead V1 0.26 0.19R-wave duration index in lead V2 0.45 0.33R-/S-wave amplitude index 0.20 0.15Precordial QRS transition V2-V3 V3

QRS morphology in lead I R RR'QRS morphology in lead aVL RR' QSQRS morphology in lead aVR QS QSQRS morphology in II, III, aVF R, R, R R, R, R

Discussion

Although the RVOT is the classic site for idiopathic VTsor PVCswith LBBBmorphology and inferior axis, these VTscan also be ablated from nearby structures, including theaortic sinuses of Valsalva, great cardiac vein, and epicardialleft ventricular outflow region.1-4 Ventricular arrhythmiasoriginating from the RCC and the NCC can mimic the ECGand electrophysiologic features of the VTs arising from theRV His bundle region.2 Most of the idiopathic VTs or PVCsoriginating from aortic root are ablated at the commissure

between the RCC and the left coronary cusp (LCC), the LCC,the RCC, and rarely the NCC.4

Electrocardiographic characteristics and origin of theventricular arrhythmia

The unique finding of the present report was the detailedevaluation of the ECG characteristics of the NCC VT. Wefound that the ECG characteristics of the NCC VT weremore similar to the ventricular arrhythmias of the RV Hisbundle origin than those of the aortic sinuses of Valsalva.Both patients had R/S amplitude index less than 0.3, R-wave

Fig. 4. Local EGMs and catheter positions at the successful ablation site in case 2. A, First beat is sinus, and second and third beats are first 2 beats of VT. Hipotential is clearly recorded in sinus beat. Both sinus and VT beat show a large atrial potential and a small multicomponent ventricular potential. During VT, theablation catheter recorded an early fractionated ventricular potential (preceding the QRS onset by 52 ms). B and C, Aortogram in left anterior oblique and righanterior oblique views clearly illustrated catheter positions within the NCC. II, V1, and V3 indicate surface ECG leads; HRA-D, the distal electrode pair of thecatheter placed in high right atrium; HIS-D, the distal electrode pair of the catheter placed in RV His bundle region; ABL-D, the distal electrode pair of theablation catheter; ABL Uni, the distal unipolar electrode of the ablation catheter; HRA, catheter at high right atrium; HIS, His bundle catheter; RVA, RV catheteat apex; ABL, ablation catheter; CS, coronary sinus catheter; PIG, pigtail catheter; LCA, left main coronary artery; RCA, right coronary artery.

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duration index less than 0.5 in precordial leads V1 throughV2, and R or RR' in lead I (Table 1). According to thealgorithm developed by Ito et al,5 these ECG characteristicsare in favor of the outflow tract VTs originating near the RVHis bundle. This finding can be explained by the anatomicalproximity of the NCC to the His bundle region.

s

t

r

Previous studies

Although there are several reports of the successfulablation of the atrial tachycardia and the anteroseptalaccessory pathway in the NCC,6-9 this cusp has rarelybeen reported as the location of the idiopathic VTs or PVCs.

175S. Sayah et al. / Journal of Electrocardiology 45 (2012) 170–175

Yamada et al2 recently reported the ECG characteristics ofthe idiopathic VTs originating in the vicinity of the Hisbundle. In this series of 13 patients, the NCC was thetachycardia origin only in 1 patient. In this report, NCC VTexhibited LBBB morphology, left inferior axis, precordialtransition between V2 and V3, and positive QRS in leads Iand aVL. Our first patient exhibited similar ECG character-istics. The QS morphology in aVL in our second patient maybe in consequence of the fact that VT origin was close to thecommissure between NCC and LCC. We observed anotched R-wave in lead I in the second patient; a similarfinding was reported by Kanagaratnam et al10 in 1 patientwith NCC VT. Alasady et al11 presented another series of 2patients with frequent symptomatic NCC PVCs. Theseauthors reported a bifid QRS morphology in V1, precordialtransition before V2, and a negative QRS in lead aVL as thetypical ECG features of NCC PVC. These discrepanciesmay be caused by the fact that there are several atypicalfindings for VTs or PVCs originating from the NCC in thisreport. First, both patients had ventricular capture from theearliest activation site; however, ventricular capture is hardlypossible from the NCC considering that there is noanatomical relationship between the NCC and the ventric-ular myocardium. In an interesting study by Lin et al,12

pacing from the NCC uniformly resulted in atrial capture. Asimilar finding was observed in the Yamada series and ourpatients. Second, the successful ablation sites showed asmall atrial and a large ventricular electrograms (EGM).Considering the anatomical relationships of the NCC, a largeatrial and a small fractionated ventricular EGM are expectedat this region.13

Conclusions and clinical implications

In case of the idiopathic outflow tract VTs or PVCswith an earliest activation in the RV His bundle regionand suggestive ECG characteristics, early aortic rootmapping is recommended to find the optimal site forablation. An imaging modality (aortography and transeso-phageal or intracardiac echocardiography) can be helpfulin guiding the ablation catheter and in assessing theanatomical relationship between the aorta and thesurrounding structures.

References

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2. Yamada T, McElderry HT, Doppalapudi H, Kay GN. Catheter ablationof ventricular arrhythmias originating from the vicinity of the Hisbundle: significance of mapping of the aortic sinus cusp. Heart Rhythm2008;5:37.

3. Yamada T, McElderry HT, Doppalapudi H, et al. Idiopathic ventriculararrhythmias originating from the aortic root prevalence, electrocardio-graphic and electrophysiologic characteristics, and results of radio-frequency catheter ablation. J Am Coll Cardiol 2008;52:139.

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11. Alasady M, Singleton CB, McGavigan AD. Left ventricular outflowtract ventricular tachycardia originating from the noncoronary cusp:electrocardiographic and electrophysiological characterization andradiofrequency ablation. J Cardiovasc Electrophysiol 2009;20:1287.

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