title: Contraction delay of the RV outflow tract in patients with Brugada syndrome is dependent on the spontaneous ST-segment elevation pattern.
abstract: BACKGROUND
  A growing body of evidence suggests that the arrhythmogenic substrate underlying Brugada syndrome (BrS) is located in the right ventricular outflow tract (RVOT), and electrophysiological abnormalities recently evidenced most commonly concur in conduction slowing. Also, imaging studies reported wall motion abnormalities of the RVOT in patients with BrS, with a various extent of RV remodeling. However, there are no data regarding a potential relationship between electrophysiological alterations and contraction abnormalities in BrS.
  
  
  OBJECTIVE
  We aimed to assess (1) the potential relationship between contraction delays of the RV quantified by phase analysis of equilibrium radionuclide angiography (ERNA), and the spontaneous ST-segment elevation pattern; and (2) to evidence RV remodeling in patients with BrS.
  
  
  METHODS
  Seventy patients with BrS and 18 control subjects were included in the study. For the purpose of the study, the spontaneous ST-segment elevation pattern was graded simultaneously to ERNA acquisition. RV contraction delays and amplitude were assessed using multiharmonic phase analysis of ERNA, and ventricular volumes and ejection fraction were assessed using gated blood-pool single photon emission computed tomography.
  
  
  RESULTS
  RVOT contraction was delayed in patients with BrS, and RV contraction heterogeneity increased according to the pattern of ST-segment elevation, without impairment of the amplitude of contraction. RV volumes were greater in patients with BrS compared with control subjects, without impairment of the ejection fraction, whatever the ST-segment elevation pattern or the magnitude of contraction heterogeneity.
  
  
  CONCLUSIONS
  In patients with BrS, we found a relationship between RV contraction heterogeneity and ST-segment pattern, providing evidence of a functional modulation of the arrhythmogenic substrate.
authors.affiliation: AP-HP, Groupe Hospitalier Bichat-Claude Bernard, Service de Médecine Nucléaire, Paris, France. francois.rouzet@bch.aphp.fr
authors.forename: François
authors.initials: F
authors.lastname: Rouzet
authors.forename: Vincent
authors.initials: V
authors.lastname: Algalarrondo
authors.forename: Samuel
authors.initials: S
authors.lastname: Burg
authors.forename: Pierre
authors.initials: P
authors.lastname: Nassar
authors.forename: Laure
authors.initials: L
authors.lastname: Sarda-Mantel
authors.forename: Philip
authors.initials: P
authors.lastname: Aouate
authors.forename: Robert
authors.initials: R
authors.lastname: Frank
authors.forename: Antoine
authors.initials: A
authors.lastname: Leenhardt
authors.forename: Véronique
authors.initials: V
authors.lastname: Fressart
authors.forename: Philippe
authors.initials: P
authors.lastname: Charron
authors.forename: Michel S
authors.initials: MS
authors.lastname: Slama
authors.forename: Dominique
authors.initials: D
authors.lastname: Le Guludec
mesh_terms: D000328:Adult; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D053840:Brugada Syndrome / Q000235:genetics / Q000503:physiopathology*; D016022:Case-Control Studies; D004247:DNA / Q000032:analysis; D004562:Electrocardiography; D005260:Female; D015637:Gated Blood-Pool Imaging; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D062554:NAV1.5 Voltage-Gated Sodium Channel; D015222:Sodium Channels / Q000235:genetics; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology*; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology*
chemical_list: D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D015222:Sodium Channels; D004247:DNA