title: Hydroquinidine therapy in Brugada syndrome.
abstract: OBJECTIVE
  We sought to assess hydroquinidine (HQ) efficacy in selected patients with Brugada syndrome (BrS).
  
  
  BACKGROUND
  Management of asymptomatic patients with BrS and inducible arrhythmias remains a key issue. Effectiveness of class Ia antiarrhythmic drugs, which inhibit the potassium transient outward current of the action potential, has been suggested in BrS.
  
  
  METHODS
  From a cohort of 106 BrS patients, we studied 35 who received HQ (32 men; mean age 48 +/- 11 years). Patients had asymptomatic BrS and inducible arrhythmia (n = 31) or multiple appropriate shocks from an implantable cardioverter-defibrillator (ICD) (n = 4). Asymptomatic patients with inducible arrhythmia underwent electrophysiologic (EP)-guided therapy. When ventricular tachycardia (VT)/ventricular fibrillation (VF) inducibility was not prevented, or in case of HQ intolerance, an ICD was placed.
  
  
  RESULTS
  Hydroquinidine prevented VT/VF inducibility in 76% of asymptomatic patients who underwent EP-guided therapy. Syncope occurred in two of the 21 patients who received long-term (17 +/- 13 months) HQ therapy (1 syncope associated with QT interval prolongation and 1 unexplained syncope associated with probable noncompliance). In asymptomatic patients who received an ICD (n = 10), one appropriate shock occurred during a follow-up period of 13 +/- 8 months. In patients with multiple ICD shocks, HQ prevented VT/VF recurrence in all cases during a mean follow-up of 14 +/- 8 months.
  
  
  CONCLUSIONS
  Hydroquinidine therapy prevented VT/VF inducibility in 76% of asymptomatic patients with BrS and inducible arrhythmia, as well as VT/VF recurrence in all BrS patients with multiple ICD shocks. These preliminary data suggest that preventive treatment by HQ may be an alternative strategy to ICD placement in asymptomatic patients with BrS and inducible arrhythmia.
authors.affiliation: Amiens-Picardie University Hospital, Amiens, France. hermida.jean-sylvain@chu-amiens.fr
authors.forename: Jean-Sylvain
authors.initials: JS
authors.lastname: Hermida
authors.forename: Isabelle
authors.initials: I
authors.lastname: Denjoy
authors.forename: Jérôme
authors.initials: J
authors.lastname: Clerc
authors.forename: Fabrice
authors.initials: F
authors.lastname: Extramiana
authors.forename: Geneviève
authors.initials: G
authors.lastname: Jarry
authors.forename: Paul
authors.initials: P
authors.lastname: Milliez
authors.forename: Pascale
authors.initials: P
authors.lastname: Guicheney
authors.forename: Stefania
authors.initials: S
authors.lastname: Di Fusco
authors.forename: Jean-Luc
authors.initials: JL
authors.lastname: Rey
authors.forename: Bruno
authors.initials: B
authors.lastname: Cauchemez
authors.forename: Antoine
authors.initials: A
authors.lastname: Leenhardt
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000188:drug therapy*; D015331:Cohort Studies; D016757:Death, Sudden, Cardiac / Q000209:etiology / Q000517:prevention & control; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D011802:Quinidine / Q000031:analogs & derivatives* / Q000627:therapeutic use*; D016896:Treatment Outcome; D014693:Ventricular Fibrillation / Q000209:etiology / Q000517:prevention & control
chemical_list: D000889:Anti-Arrhythmia Agents; C014486:hydroquinidine; D011802:Quinidine