title: The electrophysiologic mechanism of ST-segment elevation in Brugada syndrome.
abstract: OBJECTIVE
  We sought to demonstrate the electrophysiologic (EP) mechanism of the ST-T change in Brugada syndrome.
  
  
  BACKGROUND
  Brugada syndrome is characterized by various electrocardiographic manifestations (e.g., right bundle branch block, ST-segment elevation, and terminal T-wave inversion in the right precordial leads) and sudden cardiac death caused by ventricular fibrillation. Direct evidence in support of the EP mechanism underlying this intriguing syndrome has been lacking.
  
  
  METHODS
  Monophasic action potentials (MAPs) were obtained from three patients with the coved-type ST-segment elevation (Brugada patients) and five control patients using the contact electrode method. Epicardial MAPs were recorded during open-chest surgery in all patients.
  
  
  RESULTS
  A spike-and-dome configuration was documented from epicardial sites of the right ventricular (RV) outflow tract in all Brugada patients but not in control patients. Monophasic action potential recordings from the endocardium with special focus on the RV outflow tract could not demonstrate any morphological abnormalities in three Brugada patients.
  
  
  CONCLUSIONS
  The presence of a deeply notched action potential in the RV epicardium, but not in endocardium, would be expected to induce a transmural current that would contribute to elevation of the ST-segment in the right precordial leads. The spike-and-dome configuration may also prolong the epicardial action potential, thus contributing to a rapid reversal of the transmural gradients and inscription of an inverted T-wave.
authors.affiliation: Division of Cardiology, National Cardiovascular Center, 5-7-1 Fujishiro-dai, Suita, Osaka 565-8565, Japan. kuritat@hsp.ncvc.go.jp
authors.forename: Takashi
authors.initials: T
authors.lastname: Kurita
authors.forename: Wataru
authors.initials: W
authors.lastname: Shimizu
authors.forename: Masashi
authors.initials: M
authors.lastname: Inagaki
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Suyama
authors.forename: Atsushi
authors.initials: A
authors.lastname: Taguchi
authors.forename: Kazuhiro
authors.initials: K
authors.lastname: Satomi
authors.forename: Naohiko
authors.initials: N
authors.lastname: Aihara
authors.forename: Shiro
authors.initials: S
authors.lastname: Kamakura
authors.forename: Junjiro
authors.initials: J
authors.lastname: Kobayashi
authors.forename: Yoshio
authors.initials: Y
authors.lastname: Kosakai
mesh_terms: D000368:Aged; D002037:Bundle-Branch Block / Q000235:genetics / Q000503:physiopathology*; D016022:Case-Control Studies; D004562:Electrocardiography; D004594:Electrophysiology; D006329:Heart Conduction System / Q000503:physiopathology*; D006331:Heart Diseases / Q000503:physiopathology / Q000601:surgery; D006801:Humans; D008297:Male; D008875:Middle Aged; D009154:Mutation; D062554:NAV1.5 Voltage-Gated Sodium Channel; D012107:Research Design; D015222:Sodium Channels / Q000235:genetics; D013577:Syndrome; D013610:Tachycardia / Q000503:physiopathology
chemical_list: D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels