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Ventricular Fibrillation Induced by a Narrow QRS ComplexTachycardia in a Patient with Brugada Syndrome

TAKAYUKI NAGAI, M.D.,∗ WATARU SHIMIZU, M.D.,† AKIYOSHI OGIMOTO, M.D.,∗

JITSUO HIGAKI, M.D.,∗ and HIDEKI OKAYAMA, M.D.∗

From the ∗Division of Cardiology, Department of Integrated Medicine and Informatics, Ehime University Graduate School of Medicine,Ehime, Japan; and †Division of Cardiology, Department of Internal Medicine, National Cardiovascular Center, Suita, Osaka, Japan

A 50-year-old woman was successfully resuscitated fromspontaneous ventricular fibrillation (VF). She had not ex-perienced a syncopal attack before and was not taking anymedication. Her son died suddenly at the age of 20 years.No structural abnormalities were detected by echocardio-graphy. The episode of VF was recorded by chance on

J Cardiovasc Electrophysiol, Vol. 20, pp. 106-107, January 2009.

Drs. Nagai and Shimizu contributed equally to this work.

Address for correspondence: Takayuki Nagai, M.D., Division of Cardiol-ogy, Department of Integrated Medicine and Informatics, Ehime UniversityGraduate School of Medicine, Shitsukawa, Toon, Ehime, 791-0295, Japan.Fax: +81-89-960-5306; E-mail: nagait@m.ehime-u.ac.jp

doi: 10.1111/j.1540-8167.2008.01235.x

24-hour Holter ECG, which was conducted for evaluationof paroxysmal atrial fibrillation (AF) documented 1 monthbefore. According to the two-channel ECG recording, parox-ysmal AF occurred during walking in the daytime and con-verted to a regular narrow QRS complex tachycardia at arate of 240 beats/min, probably atrial flutter with 1:1 atri-oventricular conduction (Fig. 1A). Soon after the rhythmdegenerated into VF, hemodynamic collapse developed(Fig. 1B).

Her 12-lead ECG showed sinus rhythm with prolongedP-wave (140 ms) and QRS (136 ms) duration, and spon-taneous type 1 coved-type ST-segment elevation in V1-V3precordial leads recorded at a higher intercostal space (3rdand 2nd intercostal space at V1 and V2 leads), but not in thenormal intercostal space (Fig. 2).1 Molecular genetic screen-ing identified a de novo missense mutation (R121W) in theSCN5A gene, confirming the diagnosis of Brugada syndrome

Nagai et al. Narrow QRS Tachycardia-Induced VF 107

(BrS). An implantable cardioverter-defirillator was subse-quently implanted.

Mutations in the SCN5A gene have been found to be re-sponsible for other cardiac rhythm disorders, including longQT syndrome, isolated conduction disorder, sick sinus syn-drome, and AF.2,3 Eckardt et al. demonstrated that almostone-third of patients with BrS had supraventricular tach-yarrhythmias (SVT).4 However, an induction of VF by fastSVT, atrial flutter in this case, has not been reported previ-ously in BrS.

References

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2. Terrenoire C, Simhaee D, Kass RS: Role of sodium channels in prop-agation in heart muscle: How subtle genetic alterations result in ma-jor arrhythmic disorders. J Cardiovasc Electrophysiol 2007;18:900-905.

3. Darbar D, Kannankeril PJ, Donahue BS, Kucera G, Stubblefield T,Haines JL, George AL Jr, Roden DM: Cardiac sodium channel (SCN5A)variants associated with atrial fibrillation. Circulation 2008;117:1927-1935.

4. Eckardt L, Kirchhof P, Loh P, Schulze-Bahr E, Johna R, Wichter T,Breithardt G, Haverkamp W, Borggrefe M: Brugada syndrome andsupraventricular tachyarrhythmias: A novel association? J CardiovascElectrophysiol 2001;12:680-685.