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Failure of Cilostazol in the Prevention of Ventricular Fibrillation in a Patient with Brugada Syndrome
ATILIO ABUD, M.D.*, DANIEL BAGATTIN, M.D.*, RAUL GOYENECHE, M.D.*, and CARLOS BECKER, M.D.*
From the   *Cardiology Department, San Gerónimo Clinic, Santa Fé, Argentina
Correspondence to  Atilio Marcelo Abud, M.D., Crespo 2001, 3000 Santa Fe, Argentina. Fax: 54-342-4553650; E-mail: mabud@gigared.com

Manuscript received 7 April 2005; Revised manuscript received 1 June 2005; Accepted for publication 3 June 2005.

Copyright 2005 by Futura Publishing Company, Inc.
KEYWORDS
Brugada syndromeventricular fibrillationcilostazol

Cilostazol Does Not Prevent VF in Brugada Syndrome. 

(J Cardiovasc Electrophysiol, Vol. 17, pp. 210-212, February 2006)

ABSTRACT

The ECG appearance in Brugada syndrome is caused by failure of the dome of the action potential to develop. Increased activity of the I(to) current in epicardial cells generates a transmural gradient with repolarization dispersion between the epicardium and the endocardium in the right ventricular wall, thus favoring the development of VF by a phase 2 reentry mechanism. The efficacy of cilostazol for the management of these arrhythmias has been reported. This drug is a phosphodiesterase inhibitor with positive chronotropic properties, thus blocking outward potassium currents I(to) in the myocardial tissue. We present a patient with Brugada syndrome with an implantable cardioverter defibrillator (ICD), who suffered multiple ICD discharges due to VF during therapy with this drug.


Received: 07 April 2005; First Revision: 01 June 2005; Accepted: 03 June 2005;
DIGITAL OBJECT IDENTIFIER (DOI)
10.1111/j.1540-8167.2005.00290.x About DOI

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