title: Abnormal restitution property of action potential duration and conduction delay in Brugada syndrome: both repolarization and depolarization abnormalities.
abstract: OBJECTIVE
  This study sought to examine the action potential duration restitution (APDR) property and conduction delay in Brugada syndrome (BrS) patients. A steeply sloped APDR curve and conduction delay are known to be important determinants for the occurrence of ventricular fibrillation (VF).
  
  
  RESULTS
  Endocardial monophasic action potential was obtained from 39 BrS patients and 9 control subjects using the contact electrode method. Maximum slopes of the APDR curve were obtained at both the right ventricular outflow tract (RVOT) and the right ventricular apex (RVA). The onset of activation delay (OAD) after premature stimulation was examined as a marker of conduction delay. Maximum slope of the APDR curve in BrS patients was significantly steeper than that in control subjects at both the RVOT and the RVA (0.77 +/- 0.21 vs. 058 +/- 0.14 at RVOT, P = 0.009; 0.98 +/- 0.23 vs. 0.62 +/- 0.16 at RVA, P = 0.001). The dispersion of maximum slope of the APDR curve between the RVOT and the RVA was also larger in BrS patients than in control subjects. The OAD was significantly longer in BrS patients than in control subjects from the RVOT to RVA and from the RVA to RVOT (from RVOT to RVA: 256 +/- 12 vs. 243 +/- 7 ms, P = 0.003; from RVA to RVOT: 252 +/- 11 vs. 241 +/- 9 ms, P = 0.01).
  
  
  CONCLUSIONS
  Abnormal APDR properties and conduction delay were observed in BrS patients. Both repolarization and depolarization abnormalities are thought to be related to the development of VF in BrS patients.
authors.affiliation: Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan. nnishii@md.okayama-u.ac.jp
authors.forename: Nobuhiro
authors.initials: N
authors.lastname: Nishii
authors.forename: Satoshi
authors.initials: S
authors.lastname: Nagase
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Morita
authors.forename: Kengo Fukushima
authors.initials: KF
authors.lastname: Kusano
authors.forename: Tsunetoyo
authors.initials: T
authors.lastname: Namba
authors.forename: Daiji
authors.initials: D
authors.lastname: Miura
authors.forename: Kohei
authors.initials: K
authors.lastname: Miyaji
authors.forename: Shigeki
authors.initials: S
authors.lastname: Hiramatsu
authors.forename: Takeshi
authors.initials: T
authors.lastname: Tada
authors.forename: Masato
authors.initials: M
authors.lastname: Murakami
authors.forename: Atsuyuki
authors.initials: A
authors.lastname: Watanabe
authors.forename: Kimikazu
authors.initials: K
authors.lastname: Banba
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Sakai
authors.forename: Kazufumi
authors.initials: K
authors.lastname: Nakamura
authors.forename: Takefumi
authors.initials: T
authors.lastname: Oka
authors.forename: Tohru
authors.initials: T
authors.lastname: Ohe
mesh_terms: D000200:Action Potentials / Q000502:physiology*; D000328:Adult; D000368:Aged; D053840:Brugada Syndrome / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology*; D002304:Cardiac Pacing, Artificial; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009124:Muscle Proteins / Q000235:genetics; D062554:NAV1.5 Voltage-Gated Sodium Channel; D015222:Sodium Channels / Q000235:genetics; D014693:Ventricular Fibrillation / Q000175:diagnosis / Q000235:genetics / Q000503:physiopathology*
chemical_list: D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels