Inflammation plays a key role in atrial fibrillation by inducing arrhythmogenic fibrotic changes in the myocardium, with inflammatory markers predicting treatment responses.
This review highlights the role of the inflammatory cascade in inducing arrhythmogenic fibrotic changes in atrial fibrillation, suggesting biological agents and immunomodulators as potential future therapies.
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.
Nso et al. (Wed,) conducted a review in Atrial fibrillation. Inflammation plays a key role in atrial fibrillation by inducing arrhythmogenic fibrotic changes in the myocardium, with inflammatory markers predicting treatment responses.
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