Failure of cilostazol in the prevention of ventricular fibrillation in a patient with Brugada syndrome

J Cardiovasc Electrophysiol. 2006 Feb;17(2):210-2. doi: 10.1111/j.1540-8167.2005.00290.x.

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.

Publication types

  • Case Reports

MeSH terms

  • Adult
  • Anti-Arrhythmia Agents / therapeutic use*
  • Bundle-Branch Block / therapy*
  • Cilostazol
  • Defibrillators, Implantable
  • Electrocardiography
  • Heart Rate / drug effects
  • Humans
  • Male
  • Phosphodiesterase Inhibitors / therapeutic use*
  • Syndrome
  • Tetrazoles / therapeutic use*
  • Treatment Failure
  • Ventricular Fibrillation / prevention & control*

Substances

  • Anti-Arrhythmia Agents
  • Phosphodiesterase Inhibitors
  • Tetrazoles
  • Cilostazol