Role of inflammation in atrial fibrillation: A comprehensive review of current knowledge

Nso Nso, Kaveh R Bookani, Mark Metzl, Farshid Radparvar, Nso Nso, Kaveh R Bookani, Mark Metzl, Farshid Radparvar

Abstract

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.

Keywords: atrial fibrillation; cardiac arrhythmia; inflammatory biomarkers.

Conflict of interest statement

None.

© 2020 The Authors. Journal of Arrhythmia published by John Wiley & Sons Australia, Ltd on behalf of the Japanese Heart Rhythm Society.

Figures

FIGURE 1
FIGURE 1
Major changes caused by atrial fibrillation (AF) include electrical and structural remodeling. Minute but irregular changes in electrocardiogram of AF patient can be seen in the figure. Ca2+ is the center of the electrical changes, with several more perturbations linked to it. Increased calcium leads to short refractory period (depicted by blue in the cycle), leading to transmission of re‐entrant waves, breaking normal sequence, and setting up more cycles. At tissue scale structural remodeling, conduction is slowed by the myofibroblast (represented by M) secreting collagen (shown in yellow), leading to fibrosis. Myofibroblast is involved in ionic remodeling and its interaction with cardiomyocyte (represented by C) also slackens conduction
FIGURE 2
FIGURE 2
Mitochondrial‐derived reactive oxygen species and inflammatory mediators such as interleukins, cytokines (monocytes shown in yellow, macrophages shown in red, lymphocytes in purple) etc trigger atrial fibrillation
FIGURE 3
FIGURE 3
Overview of management of the atrial fibrillation (AF). Both prevention and treatment measures are necessary for successful therapy

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