Improved understanding of the pathophysiology of atrial fibrillation through the lens of discrete pathological pathways
Atrial fibrillation (AF) is a common disorder with a complex and incompletely understood pathophysiology. Genetic approaches to understanding the pathophysiology of AF have led to the identification of several biological pathways important in the pathogenesis of the arrhythmia. These include pathways important for cardiac development, generation and propagation of atrial electrical impulses, and atrial remodeling and fibrosis. While common and rare genetic variants in these pathways are associated with increased susceptibility to AF, they differ substantially among patients with lone versus typical AF. Furthermore, how these pathways converge to a final common clinical phenotype of AF is unclear and might also vary among different patient populations. Here, we review the contemporary knowledge of AF pathogenesis and discuss how derangement in cardiac development, ion channel dysfunction, and promotion of atrial fibrosis may contribute to this common and important clinical disorder.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2014 |
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| Erschienen: |
2014 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:2014 |
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| Enthalten in: |
Global cardiology science & practice - 2014(2014), 1 vom: 01., Seite 24-36 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Balouch, Muhammad A [VerfasserIn] |
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| Links: |
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| Themen: |
Atrial fibrillation |
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| Anmerkungen: |
Date Completed 23.07.2014 Date Revised 21.10.2021 published: Electronic-eCollection Citation Status PubMed-not-MEDLINE |
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| doi: |
10.5339/gcsp.2014.5 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM240348346 |
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| 520 | |a Atrial fibrillation (AF) is a common disorder with a complex and incompletely understood pathophysiology. Genetic approaches to understanding the pathophysiology of AF have led to the identification of several biological pathways important in the pathogenesis of the arrhythmia. These include pathways important for cardiac development, generation and propagation of atrial electrical impulses, and atrial remodeling and fibrosis. While common and rare genetic variants in these pathways are associated with increased susceptibility to AF, they differ substantially among patients with lone versus typical AF. Furthermore, how these pathways converge to a final common clinical phenotype of AF is unclear and might also vary among different patient populations. Here, we review the contemporary knowledge of AF pathogenesis and discuss how derangement in cardiac development, ion channel dysfunction, and promotion of atrial fibrosis may contribute to this common and important clinical disorder | ||
| 650 | 4 | |a Journal Article | |
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| 650 | 4 | |a fibrosis | |
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