Abstract 15888: Noninvasive Evaluation of Arrhythmic Substrate in the Brugada Syndrome using High Resolution Magnetocardiography
Conduction abnormalities in the right ventricular outflow tract (RVOT) are likely to be an electrophysiological substrate of ventricular fibrillation (VF) in patients with the Brugada syndrome (BrS). We hypothesized high spatio-temporal resolution magnetocardiography (MCG) noninvasively evaluated the substrate of VT/VF in the BrS.
Methods: 64-channel MCG and 12-lead ECG were simultaneously recorded in 90 patients with BrS (45 spontaneous type-1 Brugada-ECG, 3 resuscitated from VF, 17 with syncope, and 70 asymptomatic) and 20 control subjects. We analyzed 2-D current map under baseline and after administration of pilsicainide.
Results: Patients with type-1 BrS-ECG had longer QRS duration (108±20 vs. 101±10 ms; p<0.05), larger maximum MCG current at the end of QRS (52±29 vs.41±22 pT/m: p=0.05) and longer conduction time of RVOT (66±30 vs. 41±12 ms; p<0.001) compared to the type-2 ECG patients. Na channel blocker, pilsicainide (25-50 mg) unmasked type-1 BrS-ECG as well as increased RVOT conduction (54±18 to 127±62 ms;p<0.05), whereas additional isoproterenol (1ug/kg/min) reversed the pilsicainide-induced local conduction delay (61±12 ms), thus normalized the ST-segment elevation of ECG. Most (90%) of the final RVOT current arrows were moved to the left cranial area beyond the end of QRS (Figure, red arrow) when the repolarization currents were still observed. Programmed electrical stimulation easily induced VF in BrS patients with delayed RVOT conduction (>50ms) but rare in those without delay (83% vs. 16%; p<0.05). Mutational analysis in SCN5A was performed in 23 BrS patients and 6 (26%) of them are positive (SCN5A+). QRS duration was longer in SCN5A+ patients than in SCN5A- patients, but no difference was observed in RVOT conduction time, maximum current at QRS-end between with and without SCN5A mutation.
Conclusion: MCG could noninvasively demonstrate the substrate of VF, which may help us to stratify the risk of sudden arrhythmic death in the Brugada syndrome.
- © 2012 by American Heart Association, Inc.