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Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome
BACKGROUND: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the presen...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Academy of Medical Sciences
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985285/ https://www.ncbi.nlm.nih.gov/pubmed/33754508 http://dx.doi.org/10.3346/jkms.2021.36.e75 |
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author | Yoon, Namsik Jeong, Hyung Ki Lee, Ki Hong Park, Hyung Wook Cho, Jeong Gwan |
author_facet | Yoon, Namsik Jeong, Hyung Ki Lee, Ki Hong Park, Hyung Wook Cho, Jeong Gwan |
author_sort | Yoon, Namsik |
collection | PubMed |
description | BACKGROUND: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the present study was to demonstrate RV conduction delays in BrS. METHODS: The RV outflow tract (RVOT)-to-RV apex (RVA) and RVA-to-RVOT conduction times were measured by endocardial stimulation and mapping in 7 patients with BrS and 14 controls. RESULTS: Patients with BrS had a longer PR interval (180 ± 12.6 vs. 142 ± 6.7 ms, P = 0.016). The RVA-to-RVOT conduction time was longer in the patients with BrS than in controls (stimulation at 600 ms, 107 ± 9.9 vs. 73 ± 3.4 ms, P = 0.001; stimulation at 500 ms, 104 ± 12.3 vs. 74 ± 4.2 ms, P = 0.037; stimulation at 400 ms, 107 ±12.2 vs. 73 ± 5.1 ms, P = 0.014). The RVOT-to-RVA conduction time was longer in the patients with BrS than in controls (stimulation at 500 ms, 95 ± 10.3 vs. 62 ± 4.1 ms, P = 0.007; stimulation at 400 ms, 94 ±11.2 vs. 64 ± 4.6 ms, P = 0.027). The difference in longitudinal conduction time was not significant when isoproterenol was administered. CONCLUSION: The patients with BrS showed an RV longitudinal conduction delay obviously. These findings suggest that RV conduction delay might contribute to generate the BrS phenotype. |
format | Online Article Text |
id | pubmed-7985285 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | The Korean Academy of Medical Sciences |
record_format | MEDLINE/PubMed |
spelling | pubmed-79852852021-03-31 Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome Yoon, Namsik Jeong, Hyung Ki Lee, Ki Hong Park, Hyung Wook Cho, Jeong Gwan J Korean Med Sci Original Article BACKGROUND: The mechanism of Brugada syndrome (BrS) is still unclear, with different researchers favoring either the repolarization or depolarization hypothesis. Prolonged longitudinal activation time has been verified in only a small number of human right ventricles (RVs). The purpose of the present study was to demonstrate RV conduction delays in BrS. METHODS: The RV outflow tract (RVOT)-to-RV apex (RVA) and RVA-to-RVOT conduction times were measured by endocardial stimulation and mapping in 7 patients with BrS and 14 controls. RESULTS: Patients with BrS had a longer PR interval (180 ± 12.6 vs. 142 ± 6.7 ms, P = 0.016). The RVA-to-RVOT conduction time was longer in the patients with BrS than in controls (stimulation at 600 ms, 107 ± 9.9 vs. 73 ± 3.4 ms, P = 0.001; stimulation at 500 ms, 104 ± 12.3 vs. 74 ± 4.2 ms, P = 0.037; stimulation at 400 ms, 107 ±12.2 vs. 73 ± 5.1 ms, P = 0.014). The RVOT-to-RVA conduction time was longer in the patients with BrS than in controls (stimulation at 500 ms, 95 ± 10.3 vs. 62 ± 4.1 ms, P = 0.007; stimulation at 400 ms, 94 ±11.2 vs. 64 ± 4.6 ms, P = 0.027). The difference in longitudinal conduction time was not significant when isoproterenol was administered. CONCLUSION: The patients with BrS showed an RV longitudinal conduction delay obviously. These findings suggest that RV conduction delay might contribute to generate the BrS phenotype. The Korean Academy of Medical Sciences 2021-03-08 /pmc/articles/PMC7985285/ /pubmed/33754508 http://dx.doi.org/10.3346/jkms.2021.36.e75 Text en © 2021 The Korean Academy of Medical Sciences. https://creativecommons.org/licenses/by-nc/4.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (https://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Yoon, Namsik Jeong, Hyung Ki Lee, Ki Hong Park, Hyung Wook Cho, Jeong Gwan Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title | Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title_full | Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title_fullStr | Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title_full_unstemmed | Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title_short | Right Ventricular Longitudinal Conduction Delay in Patients with Brugada Syndrome |
title_sort | right ventricular longitudinal conduction delay in patients with brugada syndrome |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985285/ https://www.ncbi.nlm.nih.gov/pubmed/33754508 http://dx.doi.org/10.3346/jkms.2021.36.e75 |
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