title: High-frequency potentials developed in wavelet-transformed electrocardiogram as a novel indicator for detecting Brugada syndrome.
abstract: BACKGROUND
  A reliable alternative method for detecting Brugada syndrome is desirable because the diagnosis of Brugada syndrome using 12-lead ECG is not optimal.
  
  
  OBJECTIVE
  The purpose of this study was to assess the usefulness of the wavelet-transformed ECG in detecting Brugada syndrome.
  
  
  METHODS
  The study consisted of 15 patients with Brugada syndrome and 15 healthy subjects (control group). The parameters on the signal-averaged ECG and the frequency components recorded from the wavelet-transformed ECG were compared between the two groups. Measurements were repeated after pilsicainide infusion in the two groups of patients, after an isoproterenol infusion following pilsicainide injection, and after administration of cilostazol in the group of patients with Brugada syndrome.
  
  
  RESULTS
  The positive rate of late potentials was 80% in the Brugada syndrome group and 0% in the control group (P <.01). The high-frequency components (80-150 Hz) were developed in the Brugada syndrome group to a greater extent than in the control group, but the low-frequency components (10-50 Hz) did not differ (mean peak power at 80 Hz; 713 +/- 36 vs 488 +/- 60, P <.001). After pilsicainide injection, high-frequency components significantly increased in both groups. However, after isoproterenol and cilostazol administration, high-frequency components significantly decreased but remained higher than in the control group (80 Hz; 655 +/- 40 vs 488 +/- 60, P <.001). The sensitivity of the development of high-frequency components in detecting Brugada syndrome was higher than that of signal-averaged ECG (100% vs 80%), but specificity remained high and similar (100% for both methods).
  
  
  CONCLUSIONS
  Abnormally high-frequency components recorded from the wavelet-transformed ECG might be a novel factor in detecting Brugada syndrome.
authors.affiliation: First Department of Internal Medicine, Nippon Medical School, Tokyo, Japan.
authors.forename: Kenji
authors.initials: K
authors.lastname: Yodogawa
authors.forename: Norishige
authors.initials: N
authors.lastname: Morita
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Kobayashi
authors.forename: Hideo
authors.initials: H
authors.lastname: Takayama
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Ohara
authors.forename: Takao
authors.initials: T
authors.lastname: Katoh
authors.forename: Teruo
authors.initials: T
authors.lastname: Takano
mesh_terms: D000200:Action Potentials / Q000187:drug effects; D000318:Adrenergic beta-Agonists; D000328:Adult; D000368:Aged; D000889:Anti-Arrhythmia Agents; D053840:Brugada Syndrome / Q000175:diagnosis* / Q000503:physiopathology; D000077407:Cilostazol; D004562:Electrocardiography / Q000187:drug effects / Q000379:methods*; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D006801:Humans; D007545:Isoproterenol; D008012:Lidocaine / Q000031:analogs & derivatives; D008297:Male; D008875:Middle Aged; D012107:Research Design; D013777:Tetrazoles; D013997:Time Factors; D014665:Vasodilator Agents
chemical_list: D000318:Adrenergic beta-Agonists; D000889:Anti-Arrhythmia Agents; D013777:Tetrazoles; D014665:Vasodilator Agents; D008012:Lidocaine; C042288:pilsicainide; D007545:Isoproterenol; D000077407:Cilostazol