TY - JOUR
T1 - Prognostic significance of the sodium channel blocker test in patients with Brugada syndrome
AU - Ueoka, Akira
AU - Morita, Hiroshi
AU - Watanabe, Atsuyuki
AU - Morimoto, Yoshimasa
AU - Kawada, Satoshi
AU - Tachibana, Motomi
AU - Miyamoto, Masakazu
AU - Nakagawa, Koji
AU - Nishii, Nobuhiro
AU - Ito, Hiroshi
N1 - Funding Information:
This study was supported by JSPS KAKENHI (15K09082 to Morita) and Tailor-made Medical Treatment Program with the BioBank Japan Project (BBJ) from Japan Agency for Medical Research and Development (AMED) (15km0305015h0101 to Morita).
Publisher Copyright:
© 2018 The Authors.
PY - 2018/5/15
Y1 - 2018/5/15
N2 - Background--A drug provocation test using a sodium channel blocker (SCB) can unmask a type 1 ECG pattern in patients with Brugada syndrome. However, the prognostic value of the results of an SCB challenge is limited in patients with non-type 1 ECG. We investigated the associations of future risk for ventricular fibrillation with SCB-induced ECG changes and ventricular tachyarrhythmias (VTAs). Methods and Results--We administered intravenous pilsicainide to 245 consecutive patients with Brugada syndrome (181 patients with spontaneous type 1 ECG, 64 patients with non-type 1 ECG). ECG parameters before and after the test and occurrence of drug-induced VTAs were evaluated. During a mean follow-up period of 113±57 months, fatal VTA events occurred in 31 patients (sudden death: n=3, ventricular tachycardia/ventricular fibrillation: n=28). Symptomatic patients and spontaneous type 1 ECG were associated with future fatal arrhythmic events. Univariable analysis of ECG parameters after the test showed that long PQ and QRS intervals, high ST level, and SCB-induced VTAs were associated with later VTA events during follow-up. Multivariable analysis showed that symptomatic patients, high ST level (V1) ≥0.3 mV after the test, and SCB-induced VTAs were independent predictors for future fatal arrhythmic events (hazard ratios: 3.28, 2.80, and 3.62, 95% confidence intervals: 1.54-7.47, 1.32-6.35, and 1.64-7.75, respectively; P < 0.05). Conclusions--SCB-induced VTAs and ST-segment augmentation are associated with an increased risk of the development of ventricular tachycardia/ventricular fibrillation events during follow-up in patients with Brugada syndrome.
AB - Background--A drug provocation test using a sodium channel blocker (SCB) can unmask a type 1 ECG pattern in patients with Brugada syndrome. However, the prognostic value of the results of an SCB challenge is limited in patients with non-type 1 ECG. We investigated the associations of future risk for ventricular fibrillation with SCB-induced ECG changes and ventricular tachyarrhythmias (VTAs). Methods and Results--We administered intravenous pilsicainide to 245 consecutive patients with Brugada syndrome (181 patients with spontaneous type 1 ECG, 64 patients with non-type 1 ECG). ECG parameters before and after the test and occurrence of drug-induced VTAs were evaluated. During a mean follow-up period of 113±57 months, fatal VTA events occurred in 31 patients (sudden death: n=3, ventricular tachycardia/ventricular fibrillation: n=28). Symptomatic patients and spontaneous type 1 ECG were associated with future fatal arrhythmic events. Univariable analysis of ECG parameters after the test showed that long PQ and QRS intervals, high ST level, and SCB-induced VTAs were associated with later VTA events during follow-up. Multivariable analysis showed that symptomatic patients, high ST level (V1) ≥0.3 mV after the test, and SCB-induced VTAs were independent predictors for future fatal arrhythmic events (hazard ratios: 3.28, 2.80, and 3.62, 95% confidence intervals: 1.54-7.47, 1.32-6.35, and 1.64-7.75, respectively; P < 0.05). Conclusions--SCB-induced VTAs and ST-segment augmentation are associated with an increased risk of the development of ventricular tachycardia/ventricular fibrillation events during follow-up in patients with Brugada syndrome.
KW - Brugada syndrome
KW - Risk stratification
KW - Sodium channel blocker
KW - Ventricular fibrillation
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U2 - 10.1161/JAHA.118.008617
DO - 10.1161/JAHA.118.008617
M3 - Article
C2 - 29748178
AN - SCOPUS:85046950671
SN - 2047-9980
VL - 7
JO - Journal of the American Heart Association
JF - Journal of the American Heart Association
IS - 10
M1 - e008617
ER -