Michel Haïssaguerre1, Koonlawee Nademanee2, Frédéric Sacher3, Ghassen Cheniti4, Mélèze Hocini3, Elodie Surget3, Rémi Dubois5, Edward Vigmond6, Olivier Bernus5. 1. Univ. Bordeaux, CRCTB U1045, Inserm, Bordeaux, France; IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France; Bordeaux University Hospital, Bordeaux, France. Electronic address: michel.haissaguerre@chu-bordeaux.fr. 2. Bumrungrad Hospital, Bangkok, Thailand. 3. Univ. Bordeaux, CRCTB U1045, Inserm, Bordeaux, France; IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France; Bordeaux University Hospital, Bordeaux, France. 4. IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France; Bordeaux University Hospital, Bordeaux, France. 5. Univ. Bordeaux, CRCTB U1045, Inserm, Bordeaux, France; IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France. 6. IHU LIRYC, Electrophysiology and Heart Modeling Institute, Bordeaux, France; Univ. Bordeaux, IMB, CNRS, Bordeaux, France.
Abstract
BACKGROUND: The Brugada pattern manifests as a spontaneous variability of the electrocardiographic marker, suggesting a variability of the underlying electrical substrate. OBJECTIVE: The purpose of this study was to investigate the response of the epicardial substrate of Brugada syndrome (BrS) to programmed ventricular stimulation and to Na blocker infusion. METHODS: We investigated 6 patients (all male; mean age 54 ± 14 years) with BrS and recurrent ventricular fibrillation. Five had no type 1 BrS electrocardiogram pattern at admission. They underwent combined epicardial-endocardial mapping using multielectrode catheters. Changes in epicardial electrograms were evaluated during single endocardial extrastimulation and after low-dose ajmaline infusion (0.5 mg/kg in 5 minutes). RESULTS: All patients had a region in the anterior epicardial right ventricle with prolonged multicomponent electrograms. Single extrastimulation prolonged late epicardial components by 59 ± 31 ms and in 4 patients abolished epicardial components at some sites, without reactivation by surrounding activated sites. These localized blocks occurred at an initial coupling interval of 335 ± 58 ms and then expanded to other sites, being observed in up to 40% of epicardial sites. Ajmaline infusion prolonged electrogram duration in all and produced localized blocks in 62% of sites in the same patients as during extrastimulation. Epicardial conduction recovery after ajmaline occurred intermittently and at discontinuous sites and produced beat-to-beat changes in local repolarization, resulting in an area of marked electrical disparity. These changes were consistent with models based on microstructural alterations under critical propagation conditions. CONCLUSION: In BrS, localized functional conduction blocks occur at multiple epicardial sites and with variable patterns, without being reactivated from the surrounding sites.
BACKGROUND: The Brugada pattern manifests as a spontaneous variability of the electrocardiographic marker, suggesting a variability of the underlying electrical substrate. OBJECTIVE: The purpose of this study was to investigate the response of the epicardial substrate of Brugada syndrome (BrS) to programmed ventricular stimulation and to Na blocker infusion. METHODS: We investigated 6 patients (all male; mean age 54 ± 14 years) with BrS and recurrent ventricular fibrillation. Five had no type 1 BrS electrocardiogram pattern at admission. They underwent combined epicardial-endocardial mapping using multielectrode catheters. Changes in epicardial electrograms were evaluated during single endocardial extrastimulation and after low-dose ajmaline infusion (0.5 mg/kg in 5 minutes). RESULTS: All patients had a region in the anterior epicardial right ventricle with prolonged multicomponent electrograms. Single extrastimulation prolonged late epicardial components by 59 ± 31 ms and in 4 patients abolished epicardial components at some sites, without reactivation by surrounding activated sites. These localized blocks occurred at an initial coupling interval of 335 ± 58 ms and then expanded to other sites, being observed in up to 40% of epicardial sites. Ajmaline infusion prolonged electrogram duration in all and produced localized blocks in 62% of sites in the same patients as during extrastimulation. Epicardial conduction recovery after ajmaline occurred intermittently and at discontinuous sites and produced beat-to-beat changes in local repolarization, resulting in an area of marked electrical disparity. These changes were consistent with models based on microstructural alterations under critical propagation conditions. CONCLUSION: In BrS, localized functional conduction blocks occur at multiple epicardial sites and with variable patterns, without being reactivated from the surrounding sites.