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In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities
OBJECTIVES: We investigate the extent to which the electrocardiographic (ECG) properties of intact Scn5a+/− mice reproduce the corresponding clinical Brugada syndrome phenotype and use this model to investigate the role of conduction and repolarization abnormalities in the arrhythmogenic mechanism....
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Churchill Livingstone
2010
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712183/ https://www.ncbi.nlm.nih.gov/pubmed/20638671 http://dx.doi.org/10.1016/j.jelectrocard.2010.05.015 |
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author | Martin, Claire A. Zhang, Yanmin Grace, Andrew A. Huang, Christopher L.-H. |
author_facet | Martin, Claire A. Zhang, Yanmin Grace, Andrew A. Huang, Christopher L.-H. |
author_sort | Martin, Claire A. |
collection | PubMed |
description | OBJECTIVES: We investigate the extent to which the electrocardiographic (ECG) properties of intact Scn5a+/− mice reproduce the corresponding clinical Brugada syndrome phenotype and use this model to investigate the role of conduction and repolarization abnormalities in the arrhythmogenic mechanism. METHODS AND RESULTS: The ECGs were obtained from anesthetized wild-type and Scn5a+/− mice, before and after administration of the known pro- and antiarrhythmic agents flecainide and quinidine. The ECG intervals were measured and their dispersions calculated. Scn5a+/− hearts showed ventricular arrhythmias, ST elevation, and conduction disorders including increased QT dispersion, accentuated by flecainide. Quinidine did not cause ventricular arrhythmias but exerted variable effects on ST segments and worsened conduction abnormalities. CONCLUSIONS: The ECG features in an Scn5a+/− mouse establish it as a suitable model for Brugada syndrome and demonstrate abnormal conduction and repolarization phenomena. Altered QT dispersion, taken to indicate increased transmural repolarization gradients, may be useful in clinical risk stratification. |
format | Online Article Text |
id | pubmed-3712183 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | Churchill Livingstone |
record_format | MEDLINE/PubMed |
spelling | pubmed-37121832013-07-17 In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities Martin, Claire A. Zhang, Yanmin Grace, Andrew A. Huang, Christopher L.-H. J Electrocardiol Article OBJECTIVES: We investigate the extent to which the electrocardiographic (ECG) properties of intact Scn5a+/− mice reproduce the corresponding clinical Brugada syndrome phenotype and use this model to investigate the role of conduction and repolarization abnormalities in the arrhythmogenic mechanism. METHODS AND RESULTS: The ECGs were obtained from anesthetized wild-type and Scn5a+/− mice, before and after administration of the known pro- and antiarrhythmic agents flecainide and quinidine. The ECG intervals were measured and their dispersions calculated. Scn5a+/− hearts showed ventricular arrhythmias, ST elevation, and conduction disorders including increased QT dispersion, accentuated by flecainide. Quinidine did not cause ventricular arrhythmias but exerted variable effects on ST segments and worsened conduction abnormalities. CONCLUSIONS: The ECG features in an Scn5a+/− mouse establish it as a suitable model for Brugada syndrome and demonstrate abnormal conduction and repolarization phenomena. Altered QT dispersion, taken to indicate increased transmural repolarization gradients, may be useful in clinical risk stratification. Churchill Livingstone 2010-09 /pmc/articles/PMC3712183/ /pubmed/20638671 http://dx.doi.org/10.1016/j.jelectrocard.2010.05.015 Text en © 2010 Elsevier Inc. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license |
spellingShingle | Article Martin, Claire A. Zhang, Yanmin Grace, Andrew A. Huang, Christopher L.-H. In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title | In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title_full | In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title_fullStr | In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title_full_unstemmed | In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title_short | In vivo studies of Scn5a+/− mice modeling Brugada syndrome demonstrate both conduction and repolarization abnormalities |
title_sort | in vivo studies of scn5a+/− mice modeling brugada syndrome demonstrate both conduction and repolarization abnormalities |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3712183/ https://www.ncbi.nlm.nih.gov/pubmed/20638671 http://dx.doi.org/10.1016/j.jelectrocard.2010.05.015 |
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