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Published on: February 26, 2013
Role of inflammation in atrial fibrillation: A comprehensive review of current knowledge
Nso Nso1, Kaveh R Bookani2, Mark Metzl2
1Department of Internal Medicine Division of Cardiology Icahn School of Medicine at Mount Sinai/Queens (Queens Hospital Center) Jamaica NY USA.
Insights
Inflammation contributes to atrial fibrillation (AF) by causing myocardial fibrosis, a process that worsens the condition. New treatments focus on immunomodulators to inhibit this inflammatory cascade.
Area of Science:
- Cardiology
- Immunology
- Pathophysiology
Background:
- Atrial fibrillation (AF) is a prevalent cardiac disorder linked to high morbidity and mortality.
- Current AF management strategies, including anti-arrhythmics and rate control, show limited efficacy.
- Inflammation plays a crucial role in AF, inducing structural changes in the atrial myocardium.
Purpose of the Study:
- To review the literature on the role of inflammation in atrial fibrillation.
- To explore the relationship between inflammatory markers, myocardial fibrosis, and AF.
- To identify potential therapeutic targets for AF treatment.
Main Methods:
- Comprehensive literature search using Google Scholar.
- Keywords included: Atrial fibrillation, inflammatory markers, myocardial fibrosis, immunomodulators.
- Inclusion criteria: English language articles; relevance assessment and collation.
Main Results:
- Elevated inflammatory markers are observed in AF patients and predict treatment response.
- Inflammation appears to originate near the pulmonary veins.
- Inflammation drives fibrotic changes in the atrial myocardium.
Conclusions:
- The inflammatory cascade promotes myocardial fibrosis, creating an arrhythmogenic cycle that perpetuates inflammation.
- Emerging treatments target the inhibition of inflammatory pathways using biological agents and immunomodulators.
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:
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:
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:
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.
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