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The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights
A number of clinical studies have reported that diabetes mellitus (DM) is an independent risk factor for Atrial fibrillation (AF). After adjustment for other known risk factors including age, sex, and cardiovascular risk factors, DM remains a significant if modest risk factor for development of AF....
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399657/ https://www.ncbi.nlm.nih.gov/pubmed/30863315 http://dx.doi.org/10.3389/fphys.2019.00135 |
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author | Bohne, Loryn J. Johnson, Dustin Rose, Robert A. Wilton, Stephen B. Gillis, Anne M. |
author_facet | Bohne, Loryn J. Johnson, Dustin Rose, Robert A. Wilton, Stephen B. Gillis, Anne M. |
author_sort | Bohne, Loryn J. |
collection | PubMed |
description | A number of clinical studies have reported that diabetes mellitus (DM) is an independent risk factor for Atrial fibrillation (AF). After adjustment for other known risk factors including age, sex, and cardiovascular risk factors, DM remains a significant if modest risk factor for development of AF. The mechanisms underlying the increased susceptibility to AF in DM are incompletely understood, but are thought to involve electrical, structural, and autonomic remodeling in the atria. Electrical remodeling in DM may involve alterations in gap junction function that affect atrial conduction velocity due to changes in expression or localization of connexins. Electrical remodeling can also occur due to changes in atrial action potential morphology in association with changes in ionic currents, such as sodium or potassium currents, that can affect conduction velocity or susceptibility to triggered activity. Structural remodeling in DM results in atrial fibrosis, which can alter conduction patterns and susceptibility to re-entry in the atria. In addition, increases in atrial adipose tissue, especially in Type II DM, can lead to disruptions in atrial conduction velocity or conduction patterns that may affect arrhythmogenesis. Whether the insulin resistance in type II DM activates unique intracellular signaling pathways independent of obesity requires further investigation. In addition, the relationship between incident AF and glycemic control requires further study. |
format | Online Article Text |
id | pubmed-6399657 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63996572019-03-12 The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights Bohne, Loryn J. Johnson, Dustin Rose, Robert A. Wilton, Stephen B. Gillis, Anne M. Front Physiol Physiology A number of clinical studies have reported that diabetes mellitus (DM) is an independent risk factor for Atrial fibrillation (AF). After adjustment for other known risk factors including age, sex, and cardiovascular risk factors, DM remains a significant if modest risk factor for development of AF. The mechanisms underlying the increased susceptibility to AF in DM are incompletely understood, but are thought to involve electrical, structural, and autonomic remodeling in the atria. Electrical remodeling in DM may involve alterations in gap junction function that affect atrial conduction velocity due to changes in expression or localization of connexins. Electrical remodeling can also occur due to changes in atrial action potential morphology in association with changes in ionic currents, such as sodium or potassium currents, that can affect conduction velocity or susceptibility to triggered activity. Structural remodeling in DM results in atrial fibrosis, which can alter conduction patterns and susceptibility to re-entry in the atria. In addition, increases in atrial adipose tissue, especially in Type II DM, can lead to disruptions in atrial conduction velocity or conduction patterns that may affect arrhythmogenesis. Whether the insulin resistance in type II DM activates unique intracellular signaling pathways independent of obesity requires further investigation. In addition, the relationship between incident AF and glycemic control requires further study. Frontiers Media S.A. 2019-02-26 /pmc/articles/PMC6399657/ /pubmed/30863315 http://dx.doi.org/10.3389/fphys.2019.00135 Text en Copyright © 2019 Bohne, Johnson, Rose, Wilton and Gillis. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology Bohne, Loryn J. Johnson, Dustin Rose, Robert A. Wilton, Stephen B. Gillis, Anne M. The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title | The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title_full | The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title_fullStr | The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title_full_unstemmed | The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title_short | The Association Between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights |
title_sort | association between diabetes mellitus and atrial fibrillation: clinical and mechanistic insights |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6399657/ https://www.ncbi.nlm.nih.gov/pubmed/30863315 http://dx.doi.org/10.3389/fphys.2019.00135 |
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