title: Changes in body surface potential distributions induced by isoproterenol and Na channel blockers in patients with the Brugada syndrome.
abstract: BACKGROUND
  The characteristics of unique ECG findings in the Brugada syndrome have not been well explained.
  
  
  METHODS
  To clarify their characteristics and mechanisms, body surface maps (BSM) were recorded from patients with the Brugada syndrome (13 cases; a mean age of 48 years) before and after administration of isoproterenol (ISP) or Na channel blockers (12 cases).
  
  
  RESULTS
  ST elevation in V1-V3 was decreased by 0.1 mV or more after ISP infusion in 8 of 11 cases and elevated after Na channel blockers in 8 of 12. In ventricular activation time (VAT) isochronal map, delayed conduction was noted on upper anterior chest in 11 and on anterior left chest in two. Delayed conduction areas were decreased by ISP and expanded by Na channel blockers. QRST isointegral map showed normal findings in baseline with minimal changes after ISP or Na channel blockers. Activation recovery interval (ARI) isochronal map showed prolonged area on upper anterior chest in baseline, being reduced by ISP and expanded by Na channel blockers. ARI dispersion (ARI-d), defined as difference between the maximum and minimum value of ARI, was larger in Brugada patients than that of normal subjects in baseline, and decreased after ISP and increased after Na channel blockers.
  
  
  CONCLUSIONS
  ST elevation in the Brugada syndrome is primarily caused by abnormality in depolarization rather than in repolarization. BSM can provide better information to clarify a mechanism of ECG changes adding its diagnostic value for this unique syndrome.
authors.affiliation: Department of Human Ontogeny and Childhood Development/Pediatrics, Graduate School of Medicine, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan. izumida-circ@umin.ac.jp
authors.forename: Naomi
authors.initials: N
authors.lastname: Izumida
authors.forename: Yuh
authors.initials: Y
authors.lastname: Asano
authors.forename: Shouzaburoh
authors.initials: S
authors.lastname: Doi
authors.forename: Hiroko
authors.initials: H
authors.lastname: Wakimoto
authors.forename: Seiji
authors.initials: S
authors.lastname: Fukamizu
authors.forename: Takuro
authors.initials: T
authors.lastname: Kimura
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Ueyama
authors.forename: Harumizu
authors.initials: H
authors.lastname: Sakurada
authors.forename: Seiko
authors.initials: S
authors.lastname: Kawano
authors.forename: Tohru
authors.initials: T
authors.lastname: Sawanobori
authors.forename: Masayasu
authors.initials: M
authors.lastname: Hiraoka
mesh_terms: D000318:Adrenergic beta-Agonists / Q000494:pharmacology*; D000328:Adult; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D018780:Body Surface Potential Mapping / Q000187:drug effects*; D002037:Bundle-Branch Block / Q000175:diagnosis / Q000503:physiopathology*; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D005260:Female; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology*; D008297:Male; D008875:Middle Aged; D013577:Syndrome; D014693:Ventricular Fibrillation / Q000175:diagnosis / Q000503:physiopathology*
chemical_list: D000318:Adrenergic beta-Agonists; D000889:Anti-Arrhythmia Agents; D002121:Calcium Channel Blockers; D007545:Isoproterenol