title: Local depolarization abnormalities are the dominant pathophysiologic mechanism for type 1 electrocardiogram in brugada syndrome a study of electrocardiograms, vectorcardiograms, and body surface potential maps during ajmaline provocation.
abstract: OBJECTIVE
  We sought to obtain new insights into the pathophysiologic basis of Brugada syndrome (BrS) by studying changes in various electrocardiographic depolarization and/or repolarization variables that occurred with the development of the signature type 1 BrS electrocardiogram (ECG) during ajmaline provocation testing.
  
  
  BACKGROUND
  BrS is associated with sudden cardiac death. Its pathophysiologic basis, although unresolved, is believed to reside in abnormal cardiac depolarization or abnormal repolarization.
  
  
  METHODS
  Ajmaline provocation was performed in 269 patients suspected of having BrS with simultaneous recording of ECGs, vectorcardiograms, and 62-lead body surface potential maps.
  
  
  RESULTS
  A type 1 ECG was elicited in 91 patients (BrS patients), 162 patients had a negative test result (controls), and 16 patients had an abnormal test result. Depolarization abnormalities were more prominent in BrS patients and were mapped to the right ventricle (RV) by longer right precordial filtered QRS complex durations (142 +/- 23 ms vs. 125 +/- 14 ms, p < 0.01) and right terminal conduction delay (60 +/- 11 ms vs. 53 +/- 9 ms, p < 0.01). Repolarization abnormalities remained concordant with depolarization abnormalities as indicated by steady low nondipolar content (12 +/- 8% vs. 8 +/- 4%, p = NS), lower spatial QRS-T integrals (33 +/- 12 mV.ms vs. 40 +/- 16 mV.ms, p < 0.05), similar spatial QRS-T angles (92 +/- 39 degrees vs. 87 +/- 31 degrees , p = NS), similar T(peak)-T(end) interval (143 +/- 36 ms vs. 138 +/- 25 ms, p = NS), and similar T(peak)-T(end) dispersion (47 +/- 37 ms vs. 45 +/- 27 ms, p = NS).
  
  
  CONCLUSIONS
  The type 1 BrS ECG is characterized predominantly by localized depolarization abnormalities, notably (terminal) conduction delay in the RV, as assessed with complementary noninvasive electrocardiographic techniques. We could not define a separate role for repolarization abnormalities but suggest that the typical signs of repolarization derangements seen on the ECG are secondary to these depolarization abnormalities.
authors.affiliation: Department of Cardiology, Academic Medical Center, Amsterdam, the Netherlands.
authors.forename: Pieter G
authors.initials: PG
authors.lastname: Postema
authors.forename: Pascal F H M
authors.initials: PF
authors.lastname: van Dessel
authors.forename: Jan A
authors.initials: JA
authors.lastname: Kors
authors.forename: Andre C
authors.initials: AC
authors.lastname: Linnenbank
authors.forename: Gerard
authors.initials: G
authors.lastname: van Herpen
authors.forename: Henk J
authors.initials: HJ
authors.lastname: Ritsema van Eck
authors.forename: Nan
authors.initials: N
authors.lastname: van Geloven
authors.forename: Jacques M T
authors.initials: JM
authors.lastname: de Bakker
authors.forename: Arthur A M
authors.initials: AA
authors.lastname: Wilde
authors.forename: Hanno L
authors.initials: HL
authors.lastname: Tan
mesh_terms: D000328:Adult; D000404:Ajmaline; D000889:Anti-Arrhythmia Agents; D018780:Body Surface Potential Mapping; D053840:Brugada Syndrome / Q000175:diagnosis* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged
chemical_list: D000889:Anti-Arrhythmia Agents; D000404:Ajmaline