ventricular tachycardia associated with bidirectional reentrant circuit around the tricuspid annulus...
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Ventricular Tachycardia Associated with BidirectionalReentrant Circuit Around the Tricuspid Annulusin Arrhythmogenic Right Ventricular DysplasiaTAKASHI NODA, KAZUHIRO SUYAMA, WATARU SHIMIZU, KAZUHIRO SATOMI,KIYOSHI OTOMO, EIICHIRO NAKAGAWA, TAKASHI KURITA, NAOHIKO AIHARA,and SHIRO KAMAKURAFrom the Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Suita, Japan
NODA, T., ET AL.: Ventricular Tachycardia Associated with Bidirectional Reentrant Circuit Around theTricuspid Annulus in Arrhythmogenic Right Ventricular Dysplasia. This case report describes two dis-tinct morphological ventricular tachycardias (VTs) associated with bidirectional reentrant circuit aroundthe tricuspid annulus in a 32-year-old patient with arrhythmogenic right ventricular dysplasia. Multi-ple radiofrequency linear ablation could abolish both VTs, and this patient has been clinically free fromsymptoms of VTs at 1-year follow-up. (PACE 2003; 26:2050–2051)
ventricular tachycardia, ARVD, CARTO, ablation
Case ReportA 32-year-old man was referred to our hospi-
tal for recurrent episodes of ventricular tachycar-dias (VTs). He had first symptoms with palpitationand dizziness due to VTs at 30 years of age, andhe was receiving 400 mg of amiodarone daily forthe last 2 years as therapy for VTs. His standard12-lead electrocardiogram, during sinus rhythm,showed incomplete right bundle branch block, ep-silon waves, and inverted T waves in leads V1 toV4. Clinically, he had two distinct morphologicalVTs. The morphology of the first VT was left bun-dle branch block (LBBB) morphology with a supe-rior QRS-axis deviation (Fig. 1A), while the secondVT was LBBB morphology with an inferior QRS-axis deviation (Fig. 1B).
Further examination including cardiac an-giograms, echocardiograms, magnetic resonanceimaging, and radionuclide scintigraphy, indicatedsevere right ventricular (RV) dilatation and re-duction of RV ejection fraction with no leftventricular involvement. He was diagnosed ar-rhythmogenic right ventricular dysplasia (ARVD)based on the criteria of international registry onARVD,1,2 and underwent an electrophysiologicalstudy with a three-dimensional electroanatomicmapping system (CARTO, Biosense Webster, John-son & Johnson).3,4 During sinus rhythm, the RVactivation map by CARTO showed multiple de-layed potentials in the posterolateral free wall of
Address for reprints: Kazuhiro Suyama, M.D., Division ofCardiology, Department of Internal Medicine, National Car-diovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka, 565-8565Japan. Fax: 81-6-6872-7486; e-mail: [email protected]
Received February 13, 2003; revised April 3, 2003; acceptedMay 3, 2003.
the RV near the tricuspid annulus (TA), and theRV bipolar voltage map indicated the diffuse areaof extremely reduced voltage values in the pos-terolateral free wall of the RV. Programmed elec-trical stimulation (PES) was performed from theRV free wall, and VT was induced by double ex-trastimuli. This VT was the same morphology asthe clinical first VT (LBBB morphology with a su-perior QRS-axis deviation) and was hemodynam-ically well tolerated (Fig. 1A). The RV activationmap during the VT represented the circus move-ment around the TA. In the RV free wall (Fig. 1C),the wave front of activation proceeded in a cranio-caudal direction, while it propagated in a caudo-cranial direction in the RV septal wall. Total activa-tion time was nearly equal to the VT cycle length.Resetting could be demonstrated by a single ex-trastimulus during VT, delivered from the two dif-ferent sites, not only lateral RV wall but also septalRV wall near the TA. In addition, the postpacingintervals (PPI) were equal to the VT cycle lengthat both sites. Resetting could be also shown by asingle extrastimulus delivered from the anteriorRV wall far from TA, but the PPI at this site wasmuch longer than the VT cycle length. These ob-servations indicated that the macroreentrant VTran around the TA. Radiofrequency catheter lin-ear ablation was performed during VT in the at-tempt to transect the anatomic isthmus betweenthe scar area and the TA. The first linear lesionwas created in the posterolateral free wall of theRV, but failed to interrupt the VT. Then, the sec-ond linear lesion was created in a more cranialsite resulting in termination of the VT. However,as the clinical second VT (LBBB morphology withan inferior QRS-axis deviation), the next VT wasinduced by PES (Fig. 1B). This was also hemody-namically tolerated, thus the activation mappingof VT could be performed with CARTO. The circus
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VENTRICULAR TACHYCARDIA IN ARRHYTHMOGENIC RIGHT VENTRICULAR DYSPLASIA
Figure 1. (A) Twelve-lead ECG during the first ventricular tachycardia (VT). The morphology of the first VT wasleft bundle branch block (LBBB) morphology with a superior QRS-axis deviation. (B) Twelve-lead ECG during thesecond VT. The morphology of the second VT was LBBB morphology with a superior QRS-axis deviation. (C) Theright posterior oblique view of the right ventricular (RV) activation map during the first VT by CARTO. The first VTrevolved around the tricuspid annulus (TA). Note the wavefront of activation proceeded in a cranio-caudal directionin the RV free wall. Brown dots indicate radiofrequency applications. Red dot indicates the additional radiofrequencyapplication to the gap of the second linear lesion. Gray areas represents scar (bipolar voltage amplitude ≤ 0.5 mV).(D) The right posterior oblique view of the RV activation map during the second VT by CARTO. The second VT alsorevolved around the TA. Note the wavefront of activation propagated in a reverse direction to the first VT in the RVfree wall.
movement around the TA was also shown but thewavefront of activation proceeded in the reversedirection (Fig. 1D). It was proved that the next VTwas also resulting from a reentrant circuit aroundthe TA. The additional radiofrequency application
to the gap of the second linear lesion terminatedthe VT (red dot in Fig. 1C). After this procedure,PES could not induce either VT.
The patient has been clinically free fromsymptoms of VT at 1-year follow-up.
References1. Corrado D, Fontaine G, Marcus FI, et al. Arrhythmogenic Right Ven-
tricular Dysplasia/cardiomyopathy: Need for an international reg-istry. Circulation 2000; 101:101e–106e.
2. Tada H, Shimizu W, Ohe T, et al. Usefulness of electron-beam com-puted tomography in arrhythmogenic right ventricular dysplasia.Relationship to electrophysiological abnormalities and left ventric-ular involvement. Circulation 1996; 94:437–444.
3. Boulos M, Lashevsky I, Reisner S, et al. Elec-troanatomic mapping of arrhythmogenic right ven-tricular dysplasia. J Am Coll Cardiol 2001; 38:2020–2027.
4. Ouyang F, Fotuhi P, Goya M, et al. Ventricular tachycardia aroundthe tricuspid annulus in right ventricular dysplasia. Circulation2001; 103:913–914.
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