Epicardial Adipose Tissue and Cardiac Arrhythmias: Focus on Atrial Fibrillation
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play...
Ausführliche Beschreibung
Autor*in: |
Maddalena Conte [verfasserIn] Laura Petraglia [verfasserIn] Serena Cabaro [verfasserIn] Vincenza Valerio [verfasserIn] Paolo Poggio [verfasserIn] Emanuele Pilato [verfasserIn] Emilio Attena [verfasserIn] Vincenzo Russo [verfasserIn] Adele Ferro [verfasserIn] Pietro Formisano [verfasserIn] Dario Leosco [verfasserIn] Valentina Parisi [verfasserIn] |
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Format: |
E-Artikel |
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Sprache: |
Englisch |
Erschienen: |
2022 |
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Schlagwörter: |
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Übergeordnetes Werk: |
In: Frontiers in Cardiovascular Medicine - Frontiers Media S.A., 2015, 9(2022) |
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Übergeordnetes Werk: |
volume:9 ; year:2022 |
Links: |
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DOI / URN: |
10.3389/fcvm.2022.932262 |
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Katalog-ID: |
DOAJ027438783 |
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10.3389/fcvm.2022.932262 doi (DE-627)DOAJ027438783 (DE-599)DOAJ68d47a9b12bf4555b5d82b3450849124 DE-627 ger DE-627 rakwb eng RC666-701 Maddalena Conte verfasserin aut Epicardial Adipose Tissue and Cardiac Arrhythmias: Focus on Atrial Fibrillation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. epicardial adipose tissue visceral fat inflammation atrial fibrillation fibrosis atrial remodeling Diseases of the circulatory (Cardiovascular) system Maddalena Conte verfasserin aut Laura Petraglia verfasserin aut Serena Cabaro verfasserin aut Vincenza Valerio verfasserin aut Paolo Poggio verfasserin aut Emanuele Pilato verfasserin aut Emilio Attena verfasserin aut Vincenzo Russo verfasserin aut Adele Ferro verfasserin aut Pietro Formisano verfasserin aut Dario Leosco verfasserin aut Valentina Parisi verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.932262 kostenfrei https://doaj.org/article/68d47a9b12bf4555b5d82b3450849124 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.932262/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022 |
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10.3389/fcvm.2022.932262 doi (DE-627)DOAJ027438783 (DE-599)DOAJ68d47a9b12bf4555b5d82b3450849124 DE-627 ger DE-627 rakwb eng RC666-701 Maddalena Conte verfasserin aut Epicardial Adipose Tissue and Cardiac Arrhythmias: Focus on Atrial Fibrillation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. epicardial adipose tissue visceral fat inflammation atrial fibrillation fibrosis atrial remodeling Diseases of the circulatory (Cardiovascular) system Maddalena Conte verfasserin aut Laura Petraglia verfasserin aut Serena Cabaro verfasserin aut Vincenza Valerio verfasserin aut Paolo Poggio verfasserin aut Emanuele Pilato verfasserin aut Emilio Attena verfasserin aut Vincenzo Russo verfasserin aut Adele Ferro verfasserin aut Pietro Formisano verfasserin aut Dario Leosco verfasserin aut Valentina Parisi verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.932262 kostenfrei https://doaj.org/article/68d47a9b12bf4555b5d82b3450849124 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.932262/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022 |
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10.3389/fcvm.2022.932262 doi (DE-627)DOAJ027438783 (DE-599)DOAJ68d47a9b12bf4555b5d82b3450849124 DE-627 ger DE-627 rakwb eng RC666-701 Maddalena Conte verfasserin aut Epicardial Adipose Tissue and Cardiac Arrhythmias: Focus on Atrial Fibrillation 2022 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. epicardial adipose tissue visceral fat inflammation atrial fibrillation fibrosis atrial remodeling Diseases of the circulatory (Cardiovascular) system Maddalena Conte verfasserin aut Laura Petraglia verfasserin aut Serena Cabaro verfasserin aut Vincenza Valerio verfasserin aut Paolo Poggio verfasserin aut Emanuele Pilato verfasserin aut Emilio Attena verfasserin aut Vincenzo Russo verfasserin aut Adele Ferro verfasserin aut Pietro Formisano verfasserin aut Dario Leosco verfasserin aut Valentina Parisi verfasserin aut In Frontiers in Cardiovascular Medicine Frontiers Media S.A., 2015 9(2022) (DE-627)793951607 (DE-600)2781496-8 2297055X nnns volume:9 year:2022 https://doi.org/10.3389/fcvm.2022.932262 kostenfrei https://doaj.org/article/68d47a9b12bf4555b5d82b3450849124 kostenfrei https://www.frontiersin.org/articles/10.3389/fcvm.2022.932262/full kostenfrei https://doaj.org/toc/2297-055X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 9 2022 |
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Epicardial Adipose Tissue and Cardiac Arrhythmias: Focus on Atrial Fibrillation |
abstract |
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. |
abstractGer |
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. |
abstract_unstemmed |
Atrial Fibrillation (AF) is the most frequent cardiac arrhythmia and its prevalence increases with age. AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat. |
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AF is strongly associated with an increased risk of stroke, heart failure and cardiovascular mortality. Among the risk factors associated with AF onset and severity, obesity and inflammation play a prominent role. Numerous recent evidence suggested a role of epicardial adipose tissue (EAT), the visceral fat depot of the heart, in the development of AF. Several potential arrhythmogenic mechanisms have been attributed to EAT, including myocardial inflammation, fibrosis, oxidative stress, and fat infiltration. EAT is a local source of inflammatory mediators which potentially contribute to atrial collagen deposition and fibrosis, the anatomical substrate for AF. Moreover, the close proximity between EAT and myocardium allows the EAT to penetrate and generate atrial myocardium fat infiltrates that can alter atrial electrophysiological properties. These observations support the hypothesis of a strong implication of EAT in structural and electrical atrial remodeling, which underlies AF onset and burden. The measure of EAT, through different imaging methods, such as echocardiography, computed tomography and cardiac magnetic resonance, has been proposed as a useful prognostic tool to predict the presence, severity and recurrence of AF. Furthermore, EAT is increasingly emerging as a promising potential therapeutic target. This review aims to summarize the recent evidence exploring the potential role of EAT in the pathogenesis of AF, the main mechanisms by which EAT can promote structural and electrical atrial remodeling and the potential therapeutic strategies targeting the cardiac visceral fat.</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">epicardial adipose tissue</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">visceral fat</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">inflammation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">atrial fibrillation</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">fibrosis</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">atrial remodeling</subfield></datafield><datafield tag="653" ind1=" " ind2="0"><subfield code="a">Diseases of the circulatory (Cardiovascular) 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