title: Incidence and initial characteristics of pilsicainide-induced ventricular arrhythmias in patients with Brugada syndrome.
abstract: BACKGROUND
  In patients with Brugada syndrome, class I antiarrhythmic drugs can trigger ventricular arrhythmias (VA). The incidence and initial characteristics of VA that developed after pilsicainide was examined in 28 patients with Brugada-type electrocardiographic (ECG) abnormalities and with a positive response in the pilsicainide test. The clinical outcome was also compared between patients with and without pilsicainide-induced VA.
  
  
  RESULTS
  In all patients, pilsicainide increased ST segment elevation and accentuated type 1 ECG changes. Ventricular tachycardia (VT) developed in 3 patients and premature ventricular complexes (PVC) in 2 other patients. These 5 patients (group I) had higher ST segment elevation in lead V2 on the ECG at baseline and after pilsicainide and showed a longer QTc interval after pilsicainide than the other 23 patients (group II). However, there was no difference between the 2 groups regarding incidence of prior cardiac events, results of signal-averaged ECG, HV interval, inducibility of ventricular fibrillation by programmed electrical stimulation, or QRS duration. In 1 patient, PVC originated from 3 sites, 2 of which triggered polymorphic VT. The right ventricular (RV) outflow tract was the origin of 2 types of PVC, and other RV sites of 5 other types. During a 45 +/- 37 months follow-up, polymorphic VT recurred in 2 patients in group II.
  
  
  CONCLUSIONS
  Pilsicainide induced VA in some patients with Brugada syndrome, but this result may not be used as a parameter of the risk stratification of Brugada syndrome. Multiple PVC induced by pilsicainide and triggering polymorphic VT originated from several RV sites is an important factor when considering patients for treatment with catheter ablation.
authors.affiliation: School of Health Science, Niigata University School of Medicine, Asahimachi Niigata, Japan. masaomi@clg.niigata-u.ac.jp
authors.forename: Masaomi
authors.initials: M
authors.lastname: Chinushi
authors.forename: Satoru
authors.initials: S
authors.lastname: Komura
authors.forename: Daisuke
authors.initials: D
authors.lastname: Izumi
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Furushima
authors.forename: Yasutaka
authors.initials: Y
authors.lastname: Tanabe
authors.forename: Takashi
authors.initials: T
authors.lastname: Washizuka
authors.forename: Yoshifusa
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000328:Adult; D000368:Aged; D001145:Arrhythmias, Cardiac / Q000139:chemically induced* / Q000503:physiopathology; D053840:Brugada Syndrome / Q000175:diagnosis* / Q000503:physiopathology; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006801:Humans; D015994:Incidence; D008012:Lidocaine / Q000009:adverse effects / Q000031:analogs & derivatives*; D008297:Male; D008875:Middle Aged; D026941:Sodium Channel Blockers / Q000009:adverse effects*
chemical_list: D026941:Sodium Channel Blockers; D008012:Lidocaine; C042288:pilsicainide