Longer repolarization in the epicardium at the right ventricular outflow tract causes type 1 electrocardiogram in patients with Brugada syndrome.
OBJECTIVE
We examined the relationship between repolarization abnormality and coved-type ST-segment elevation with terminal inverted T-wave (type 1 electrocardiogram [ECG]) in patients with Brugada syndrome (BrS).


BACKGROUND
Recent experimental studies have suggested that accentuation of the right ventricular action potential (AP) notch preferentially prolongs epicardial AP causing inversion of the T-wave.


METHODS
In 19 patients with BrS and 3 control subjects, activation-recovery intervals (ARIs) and repolarization times (RTs) in the epicardium and endocardium were directly examined with the use of local unipolar electrograms at the right ventricular outflow tract. Surface ECG, ARI, and RT were examined before and after administration of pilsicainide.


RESULTS
Type 1 ECG was observed in 10 of the 19 BrS patients before the administration of pilsicainide and in all of the 19 patients after the administration of pilsicainide. We found that ARI and RT in the epicardium were shorter than those in the endocardium in all 9 BrS patients without type 1 ECG under baseline conditions and in all control subjects regardless of pilsicainide administration. However, longer epicardial ARI than endocardial ARI was observed in 8 of the 10 BrS patients manifesting type 1 ECG under baseline conditions and in all of the BrS patients after the administration of pilsicainide. Also, epicardial RT was longer than endocardial RT in all patients manifesting type 1 ECG regardless of pilsicainide administration.


CONCLUSIONS
Our data provide support for the hypothesis that the negative T-wave associated with type 1 BrS ECG is due to a preferential prolongation of the epicardial AP secondary to accentuation of the AP notch in the region of the right ventricular outflow tract.
Nagase
Satoshi
S
Department of Cardiovascular Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama, Japan. snagase@cc.okayama-u.ac.jp
Kusano
Kengo Fukushima
KF
Morita
Hiroshi
H
Nishii
Nobuhiro
N
Banba
Kimikazu
K
Watanabe
Atsuyuki
A
Hiramatsu
Shigeki
S
Nakamura
Kazufumi
K
Sakuragi
Satoru
S
Ohe
Tohru
T
D000200:Action Potentials / Q000187:drug effects; D000328:Adult; D000368:Aged; D053840:Brugada Syndrome / Q000175:diagnosis / Q000503:physiopathology*; D016022:Case-Control Studies; D004562:Electrocardiography; D004699:Endocardium / Q000503:physiopathology; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology*; D006352:Heart Ventricles / Q000503:physiopathology*; D006801:Humans; D008012:Lidocaine / Q000008:administration & dosage / Q000031:analogs & derivatives; D008297:Male; D008875:Middle Aged; D010496:Pericardium / Q000503:physiopathology*; D026941:Sodium Channel Blockers / Q000008:administration & dosage
D026941:Sodium Channel Blockers; D008012:Lidocaine; C042288:pilsicainide