Inflammation and atrial fibrillation: A comprehensive review

Abstract

Atrial fibrillation (AF) has different underlying substrates. Atrial remodeling involves electrophysiological and structural abnormalities that promote the development and perpetuation of AF. Experimental and clinical data indicate that inflammation is implicated in the pathophysiology of atrial remodeling. The mechanistic links between atrial remodeling and inflammation are complex while diverse underlying diseases and conditions may affect these pathways. Inflammatory markers have also been associated with AF development, recurrence, perpetuation, total AF burden as well as with thromboembolic complications. The development of specific anti‐inflammatory interventions in this setting seems to be challenging and complicated. Several agents with pleiotropic properties, including anti‐inflammatory, have been tested in experimental and clinical settings with variable results. This updated review provides a concise overview of all available data regarding the role of inflammation in AF including the predictive role of inflammatory markers. Also, current knowledge and future directions on anti‐inflammatory strategies are critically discussed.

Galectin‐3 and risk of atrial fibrillation: A systematic review and meta‐analysis

“…It is important at the public health level because of its predisposition to stroke, heart failure, dementia, premature mortality, and disability . In this condition, there is an ongoing cardiomyopathic process of the atrial myocardium, involving a number of cellular and molecular mechanisms revolving around inflammation . One of the consequences is fibrosis, characterized by increased turnover of the extracellular matrix, producing conduction abnormalities that provide the necessary substrate for arrhythmogenesis .…”

“…52 In this condition, there is an ongoing cardiomyopathic process of the atrial myocardium, 53,54 involving a number of cellular and molecular mechanisms revolving around inflammation. 55,56 One of the consequences is fibrosis, characterized by increased turnover of the extracellular matrix, producing conduction abnormalities that provide the necessary substrate for arrhythmogenesis. 57,58 A number of blood biomarkers 3,5-7,59-62 and electrocardiographic predictors 54,63,64 have been found in association with AF onset, development, and F I G U R E 1 Flow diagram of study selection process TA B L E 1 Characteristics of included studies for meta-analysis of association of galectin-3 and AF recurrence.…”

Novel role of the clustered miR‐23b‐3p and miR‐27b‐3p in enhanced expression of fibrosis‐associated genes by targeting TGFBR3 in atrial fibroblasts

“…Meanwhile, the obvious increase of inflammatory factors, such as IL-1β and CRP, was also found in atrial appendage tissue of AF patients in the current study, which was supported by the previous reports. 28 Some miRNAs, such as miR-21 [12][13][14][15] and miR-26, 16,17 are involved in the modulation of atrial fibrosis. In this study, we demonstrated that miR-23b-3p and miR-27b-3p were increased in the human rheumatic atrial appendages and in Ang-II-induced HAFs.…”

Pharmacological Inhibition of Serine Proteases to Reduce Cardiac Inflammation and Fibrosis in Atrial Fibrillation

“…While inflammation can cause AF, AF can cause both local and generalized inflammation (Korantzopoulos, 2018). In patients with isolated forms of AF ("lone" AF), who do not have any other underlying cardiac or extracardiac AF-associated disease, atrial tissue displays a mild level of local inflammation comprising cellular infiltration (Frustaci, 1997), which appears to be a direct consequence of the arrhythmia.…”