Role of inflammation in atrial fibrillation: A comprehensive review of current knowledge.
atrial fibrillation
cardiac arrhythmia
inflammatory biomarkers
Journal
Journal of arrhythmia
ISSN: 1880-4276
Titre abrégé: J Arrhythm
Pays: Japan
ID NLM: 101263026
Informations de publication
Date de publication:
Feb 2021
Feb 2021
Historique:
received:
29
05
2020
revised:
24
10
2020
accepted:
14
11
2020
entrez:
5
3
2021
pubmed:
6
3
2021
medline:
6
3
2021
Statut:
epublish
Résumé
Atrial fibrillation (AF) is one of the most common cardiac disorders affecting adults and is associated with significant morbidity and mortality. Efforts to manage AF through anti-arrhythmics and rate control have been largely unsatisfactory. It has become clear that AF causes structural alterations in the atrial myocardium that propagate further AF, and that some of these alterations are the result of inflammation. An in-depth review of the available literature was undertaken using Google Scholar and keyword searches including [Atrial fibrillation] in combination with [inflammatory markers], [myocardial fibrosis], and [immunomodulators], limiting the search to English language articles. All articles were reviewed for relevance and collated by the author. Multiple markers of inflammation have been shown to be elevated in AF and to predict responses to treatments of AF including anti-arrhythmics and cardioversion. The nidus of inflammation is not clear but seems to be related to the pulmonary veins. The inflammatory cascade induces fibrotic changes in the myocardium, an arrhythmogenic process that stimulates further inflammation. Advances in treatment are focusing on biological agents and immunomodulators that inhibit the inflammatory cascade.
Sections du résumé
BACKGROUND
BACKGROUND
Atrial fibrillation (AF) is one of the most common cardiac disorders affecting adults and is associated with significant morbidity and mortality. Efforts to manage AF through anti-arrhythmics and rate control have been largely unsatisfactory. It has become clear that AF causes structural alterations in the atrial myocardium that propagate further AF, and that some of these alterations are the result of inflammation.
METHODS
METHODS
An in-depth review of the available literature was undertaken using Google Scholar and keyword searches including [Atrial fibrillation] in combination with [inflammatory markers], [myocardial fibrosis], and [immunomodulators], limiting the search to English language articles. All articles were reviewed for relevance and collated by the author.
RESULTS
RESULTS
Multiple markers of inflammation have been shown to be elevated in AF and to predict responses to treatments of AF including anti-arrhythmics and cardioversion. The nidus of inflammation is not clear but seems to be related to the pulmonary veins.
CONCLUSIONS
CONCLUSIONS
The inflammatory cascade induces fibrotic changes in the myocardium, an arrhythmogenic process that stimulates further inflammation. Advances in treatment are focusing on biological agents and immunomodulators that inhibit the inflammatory cascade.
Identifiants
pubmed: 33664879
doi: 10.1002/joa3.12473
pii: JOA312473
pmc: PMC7896450
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
1-10Informations de copyright
© 2020 The Authors. Journal of Arrhythmia published by John Wiley & Sons Australia, Ltd on behalf of the Japanese Heart Rhythm Society.
Déclaration de conflit d'intérêts
None.
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