IntroductionBrugada syndrome is characterized by ST-

segment elevation in leads V1–V3 and develop-ment of ventricular fibrillation (VF).1 In the pre-sent patient, self-terminating polymorphicventricular tachycardia (VT) was repetitively in-duced after administration of pilsicainide (a ClassIc antiarrhythmic drug) and initiation of the VTwas recorded on precordial electrocardiograms.

Case ReportA 50-year-old man who previously had sev-

eral episodes of chest discomfort was admitted.His electrocardiogram (ECG) on admissionshowed normal sinus rhythm and a slight ST-seg-ment elevation was observed in leads V1–V3, butthis was not typical for Brugada syndrome (Fig.1A). Results of conventional cardiac examinationwere normal. During his stay in the hospital, atrialfibrillation developed and oral pilsicainide (50mg) was administrated. Pilsicainide is a pure Nachannel blocker and is classified as a Class Ic an-tiarrhythmic drug. After the drug was given, atrialfibrillation returned to sinus rhythm but his ECGrevealed a typical configuration of Brugada syn-drome (Fig. 1B). As the magnitude of ST-segmentelevation increased, single premature ventricularcomplexes (PVCs) or couplets developed fre-quently, and self-terminating polymorphic VTswere repetitively induced following the same

PVC; QRS morphology of the VT-initiating PVCwas of a left bundle branch block pattern (Fig. 2).The coupling interval of the PVC ranged from 380to 420 ms and its initial deflection was superim-posed on the terminal portion of the T wave of thepreceding beat. The PVC or initiation of the self-terminating polymorphic VT could not berecorded in limb ECG leads during the event. Al-though PVC was infrequently recorded by HolterECG in this patient, sporadic PVC, the QRS mor-phology of which on precordial ECG leads weresimilar to that of triggered PVC, was able to berecorded on 12-lead ECG on a later day (Figs. 1Cand 2). QRS morphology of the PVC suggested thatthe origin was located in the apical area of theright ventricle.

Then, an electrophysiological study was per-formed. VF was twice induced by double or tripleextrastimulation from the right ventricle. PVC didnot develop during the electrophysiological studyand the site of PVC origin was not mapped bypacemapping. He was diagnosed as having Brugadasyndrome and a defibrillator was implanted to pre-vent possible arrhythmic events in the future.

DiscussionPrevious experimental studies have shown

that the mechanism of ST-segment elevation andinitiation of VF in Brugada syndrome are consid-ered to be due to development of greater transmu-ral dispersion of reporlarization, which facilitatesphase 2 reentry between the endocardial and epi-cardial layers of the right ventricle.2 However, thishypothesis has rarely been studied in patientswith Brugada syndrome,3 and one of the reasonsmay be related to the fact that ECG at the onset ofVF is difficult to record clinically. Recent resultsfrom the data of implantable cardioverter defibril-

Induction of Ventricular Fibrillation in BrugadaSyndrome by Site-Specific Right VentricularPremature DepolarizationMASAOMI CHINUSHI, TAKASHI WASHIZUKA,* YUKO CHINUSHI,*KOTAROU HIGUCHI,* TATUNARI TOIDA,* and YOSHIFUSA AIZAWA*From the School of Health Science and *First Department of Internal Medicine, Niigata UniversitySchool of Medicine, Asahimachi Niigata, Japan

CHINUSHI, M., ET AL.: Induction of Ventricular Fibrillation in Brugada Syndrome by Site-Specific RightVentricular Premature Depolarization. This patient was a 50-year-old man. Oral pilsicainide unmaskeda Brugada-type ECG abnormality and self-terminating polymorphic VT was repetitively induced. Thepolymorphic VT always developed following a specific ventricular premature complex showing a left bun-dle branch block pattern suggesting a limited origin in the right ventricle. (PACE 2002; 25:1649–1651)

Brugada syndrome, polymorphic VT, arrhythmogenic area

PACE, Vol. 25, No. 11 November 2002 1649

Address for reprints: Masaomi Chinushi, M.D., School ofHealth Science, Niigata University School of Medicine, 2-746Asahimachi Niigata 951-8518, Japan. Fax: (81)-25-227-0774; e-mail: masaomi 6 clg.niigata-u.ac.jp

Received December 14, 2001; revised February 19, 2002; ac-cepted March 19, 2002.

Reprinted with permission fromJOURNAL OF PACING AND CLINICAL ELECTROPHYSIOLOGY, Volume 25, No. 11, November 2002

Copyright © 2002 by Futura Publishing Company, Inc., Armonk, NY 10504-0418.

lators in Brugada syndrome suggested that VF ofBrugada syndrome could be triggered by a specificPVC.4 Since only the single ECG lead was avail-able, details of the QRS morphology that triggeredVF were not obtained in that study. In the presentcase, oral pilsicainide unmasked a Brugada-typeECG abnormality and self-terminating polymor-phic VT was repetitively initiated. Severalepisodes of the polymorphic VT on six precordialECG leads were recorded, and it was found thatthe QRS morphology of the initial beat of poly-morphic VT was almost identical in each eventshowing a left bundle branch block pattern. Fur-thermore, the PVC was superimposed on the ter-minal portion of the T wave of the preceding beat.These findings support the hypothesis from previ-ous experimental studies.2 Recording of the QRSconfiguration of PVC in limb ECG leads is impor-tant to narrow the site of PVC origin, but the PVCor polymorphic VT in limb ECG leads during the

event could not be recorded. Although sporadicPVC recorded on a later day suggested that it orig-inated from the apical area of the right ventricle, itwould be difficult to rule out the possibility of theleft ventricular septal origin because the authorscould not attempt detail mapping of the PVC dur-ing the electrophysiological study. Programmedstimulation from the site of PVC origin would pro-vide important findings about regionally differ-ences of arrhythmogenesis of Brugada syndrome,but this study was not performed in this patient.

Although the origin of the ventricular prema-ture depolarization could not be identified, the pa-tient may provide an important clinical implica-tion: specific PVC originating from a limited areaof the right ventricle may trigger spontaneousepisodes of VF in Brugada syndrome. If there is aspecific VF-initiating PVC, we may be able to treatthe electrical storm, which could possibly developafter implantation of a defibrillator device.

CHINUSHI, ET AL.

1650 November 2002 PACE, Vol. 25, No. 11

Figure 1. Twelve-lead electrocardiogram. Panel A was recorded at admission and shows onlyslight ST-segment elevation in leads V1–V3. Panel B was recorded after administration ofpilsicainide and marked ST-segment elevation was noted in leads V1–V3. Panel C was recordedon a later day and illustrated sporadic premature ventricular complexes (PVCs), the QRSmorphology of which was similar to the PVC triggered self-terminating ventricular fibrillation.

ARRHYTHMOGENIC AREA OF BRUGADA SYNDROME

PACE, Vol. 25, No. 11 November 2002 1651

Figure 2. Spontaneous initiation of polymorphic ventricular tachycardia. CI 5 coupling interval.(See details in the text.)

References1. Brugada R, Brugada J, Antzelevitch C, et al. Sodium channel block-

ers identify risk for sudden death in patients with ST segment ele-vation and right bundle branch block but structurally normal hearts.Circulation 2000; 101:510–515.

2. Yan GX, Antzelevitch C. Cellular basis for the Brugada syndromeand other mechanisms of arrhythmogenesis associated with ST-seg-ment elevation. Circulation 1999; 100:1660–1666.

3. Shimizu W, Aiba T, Kurita T, et al. Paradoxic abbreviation of repo-

larization in epicardium of the right ventricular outflow tract dur-ing augmentation of Brugada-type ST segment elevation. J Cardio-vasc Electrophysiol 2001; 12:1418–1421.

4. Kakishita M, Kurita T, Matuo K, et al. Mode of onset of ventricularfibrillation in patients with Brugada syndrome detected by im-plantable cardioverter defibrillator therapy. J Am Coll Cardiol 2000;36:1646–1653.