Simultaneous Non‐Invasive Epicardial and Endocardial Mapping in Patients With Brugada Syndrome: New Insights Into Arrhythmia Mechanisms

Background The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT)....

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Published inJournal of the American Heart Association Vol. 5; no. 11
Main Authors Rudic, Boris, Chaykovskaya, Maria, Tsyganov, Alexey, Kalinin, Vitaly, Tülümen, Erol, Papavassiliu, Theano, Dösch, Christina, Liebe, Volker, Kuschyk, Jürgen, Röger, Susanne, El‐Battrawy, Ibrahim, Akin, Ibrahim, Yakovleva, Marina, Zaklyazminskaya, Elena, Shestak, Anna, Kim, Stanislav, Chmelevsky, Mikhail, Borggrefe, Martin
Format Journal Article
LanguageEnglish
Published England John Wiley and Sons Inc 14.11.2016
Wiley
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Abstract Background The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS. Methods and Results Local epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi‐ and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation‐recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST‐segment elevation >2 mV and T‐wave inversions. Negative voltage gradient (−2.5 to −6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls. Conclusions Abnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
AbstractList Background The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract ( RVOT ). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS. Methods and Results Local epicardial and endocardial unipolar electrograms were analyzed using a novel n oninvasive e pi‐ and e ndocardial e lectrophysiology s ystem ( NEEES ) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P =0.008), prolongation of the activation‐recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P =0.002). Repolarization abnormalities included a larger area of ST ‐segment elevation >2 mV and T‐wave inversions. Negative voltage gradient (−2.5 to −6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls. Conclusions Abnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
BACKGROUNDThe underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS.METHODS AND RESULTSLocal epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi- and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation-recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST-segment elevation >2 mV and T-wave inversions. Negative voltage gradient (-2.5 to -6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls.CONCLUSIONSAbnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
BackgroundThe underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS. Methods and ResultsLocal epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi‐ and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation‐recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST‐segment elevation >2 mV and T‐wave inversions. Negative voltage gradient (−2.5 to −6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls. ConclusionsAbnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS. Local epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi- and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation-recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST-segment elevation >2 mV and T-wave inversions. Negative voltage gradient (-2.5 to -6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls. Abnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
Background The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate, leading to electrocardiogram abnormalities and/or ventricular arrhythmias, is located in the right ventricular outflow tract (RVOT). The purpose of this study was to examine abnormalities of epicardial and endocardial local unipolar electrograms by simultaneous noninvasive mapping in patients with BrS. Methods and Results Local epicardial and endocardial unipolar electrograms were analyzed using a novel noninvasive epi‐ and endocardial electrophysiology system (NEEES) in 12 patients with BrS and 6 with right bundle branch block for comparison. Fifteen normal subjects composed the control group. Observed depolarization abnormalities included fragmented electrograms in the anatomical area of RVOT endocardially and epicardially, significantly prolonged activation time in the RVOT endocardium (65±20 vs 38±13 ms in controls; P=0.008), prolongation of the activation‐recovery interval in the RVOT epicardium (281±34 vs 247±26 ms in controls; P=0.002). Repolarization abnormalities included a larger area of ST‐segment elevation >2 mV and T‐wave inversions. Negative voltage gradient (−2.5 to −6.0 mV) between epicardium and endocardium of the RVOT was observed in 8 of 12 BrS patients, not present in patients with right bundle branch block or in controls. Conclusions Abnormalities of epicardial and endocardial electrograms associated with depolarization and repolarization properties were found using NEEES exclusively in the RVOT of BrS patients. These findings support both, depolarization and repolarization abnormalities, being operative at the same time in patients with BrS.
Author Chmelevsky, Mikhail
Liebe, Volker
Röger, Susanne
Rudic, Boris
Zaklyazminskaya, Elena
Kuschyk, Jürgen
Dösch, Christina
Papavassiliu, Theano
Shestak, Anna
Chaykovskaya, Maria
Tülümen, Erol
Yakovleva, Marina
Kim, Stanislav
Kalinin, Vitaly
El‐Battrawy, Ibrahim
Akin, Ibrahim
Tsyganov, Alexey
Borggrefe, Martin
AuthorAffiliation 1 Department of Medicine University Medical Center Mannheim Mannheim Germany
4 EP Solutions SA Yverdon‐les‐Bains Switzerland
3 Petrovsky National Research Center of Surgery Moscow Russia
5 Pirogov Russian National Research Medical University Moscow Russia
2 German Center for Cardiovascular Research (DZHK) Partner Site Heidelberg/Mannheim Mannheim Germany
AuthorAffiliation_xml – name: 3 Petrovsky National Research Center of Surgery Moscow Russia
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Issue 11
Keywords sudden death
Brugada syndrome
right bundle branch block
ajmaline challenge
arrhythmia
endocardium
depolarization
repolarization
epicardium
electrocardiography
right ventricular outflow tract
Language English
License Attribution-NonCommercial-NoDerivs
2016 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
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Dr Rudic and Dr Chaykovskaya contributed equally to this article.
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Snippet Background The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological...
The underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological substrate,...
BACKGROUNDThe underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological...
BackgroundThe underlying mechanisms of Brugada syndrome (BrS) are not completely understood. Recent studies provided evidence that the electrophysiological...
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SubjectTerms Adult
Ajmaline
ajmaline challenge
Anti-Arrhythmia Agents
arrhythmia
Brugada syndrome
Brugada Syndrome - physiopathology
Bundle-Branch Block - physiopathology
Case-Control Studies
depolarization
Electrocardiography
endocardium
Endocardium - physiopathology
Epicardial Mapping
epicardium
Female
Heart - physiopathology
Heart Ventricles - physiopathology
Humans
Male
Middle Aged
Original Research
repolarization
right bundle branch block
right ventricular outflow tract
sudden death
Young Adult
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Title Simultaneous Non‐Invasive Epicardial and Endocardial Mapping in Patients With Brugada Syndrome: New Insights Into Arrhythmia Mechanisms
URI https://onlinelibrary.wiley.com/doi/abs/10.1161%2FJAHA.116.004095
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