BACKGROUND: The ECG characteristics of premature ventricular contractions (PVCs) in subjects with Brugada syndrome (BrS) phenotype were investigated. METHODS AND RESULTS: A total of 96 patients with type 1 ECG pattern of BrS were screened for PVCs. The study population consisted of 10 male individuals (mean age 41.9±5.6 years) with spontaneous (n=2) or drug-induced (n=8) type 1 ECG phenotype of BrS and PVCs. Twenty patients (11 males, age 44.6±15.1 years) with idiopathic right ventricular outflow tract (RVOT) PVCs (LBBB/inferior axis morphology with a negative QRS complex in lead aVL) successfully ablated from an endocardial site were also included in the study, and served as comparative controls. Six subjects with BrS phenotype (five during drug challenge) displayed PVCs with LBBB/inferior axis morphology and negative QRS complex in aVL lead which indicates an RVOT origin. The ECG characteristics of PVCs with LBBB/inferior axis in subjects with BrS and idiopathic RVOT arrhythmia were subsequently compared. QRS duration in inferior (p=0.001) and right precordial leads (p<0.001) was significantly longer in subjects with BrS phenotype. The RS interval in lead V2 was also significantly prolonged in individuals with BrS phenotype (p=0.016). Subjects with BrS phenotype exhibited an increased intrinsicoid deflection time measured in right precordial leads compared to those with idiopathic RVOT PVCs (46.0±7.6 vs. 27.2±9.5 ms, p<0.001). Finally, a pseudo-delta wave in precordial leads was more commonly observed in subjects with BrS ECG pattern (p=0.029). CONCLUSIONS: PVCs in BrS usually originate from the RVOT and display specific ECG characteristics that might be indicative of an epicardial origin. The prolonged interval criteria may be related to a localized epicardial conduction delay.
BACKGROUND: The ECG characteristics of premature ventricular contractions (PVCs) in subjects with Brugada syndrome (BrS) phenotype were investigated. METHODS AND RESULTS: A total of 96 patients with type 1 ECG pattern of BrS were screened for PVCs. The study population consisted of 10 male individuals (mean age 41.9±5.6 years) with spontaneous (n=2) or drug-induced (n=8) type 1 ECG phenotype of BrS and PVCs. Twenty patients (11 males, age 44.6±15.1 years) with idiopathic right ventricular outflow tract (RVOT) PVCs (LBBB/inferior axis morphology with a negative QRS complex in lead aVL) successfully ablated from an endocardial site were also included in the study, and served as comparative controls. Six subjects with BrS phenotype (five during drug challenge) displayed PVCs with LBBB/inferior axis morphology and negative QRS complex in aVL lead which indicates an RVOT origin. The ECG characteristics of PVCs with LBBB/inferior axis in subjects with BrS and idiopathic RVOT arrhythmia were subsequently compared. QRS duration in inferior (p=0.001) and right precordial leads (p<0.001) was significantly longer in subjects with BrS phenotype. The RS interval in lead V2 was also significantly prolonged in individuals with BrS phenotype (p=0.016). Subjects with BrS phenotype exhibited an increased intrinsicoid deflection time measured in right precordial leads compared to those with idiopathic RVOT PVCs (46.0±7.6 vs. 27.2±9.5 ms, p<0.001). Finally, a pseudo-delta wave in precordial leads was more commonly observed in subjects with BrS ECG pattern (p=0.029). CONCLUSIONS: PVCs in BrS usually originate from the RVOT and display specific ECG characteristics that might be indicative of an epicardial origin. The prolonged interval criteria may be related to a localized epicardial conduction delay.