Update on the Association of Inflammation and Atrial Fibrillation

Abstract

Atrial fibrillation (AF) is a common arrhythmia and is associated with significant morbidity and mortality. The pathogenesis of AF remains incompletely understood and management remains a difficult task. Over the past decade there has been accumulating evidence implicating inflammation in the pathogenesis of AF. Inflammation appears to play a significant role in the initiation and perpetuation of AF as well as the prothrombotic state associated with AF. Inflammatory biomarkers (C-reactive protein and interleukin-6) have been shown to be associated with the future development, recurrence and burden of AF, and the likelihood of successful cardioversion. Therapies directed at attenuating the inflammatory burden appear promising. Animal and clinical studies have evaluated statins, angiotensin-converting enzyme inhibitors/angiotensin-II receptor blockers, and corticosteroids for the treatment or prevention of AF. The purpose of this review is to provide current evidence on the relationship between inflammation and AF and potential therapies available to modulate the inflammatory state in AF.

Omega-3 Fatty Acids in the Prevention of Atrial Fibrillation Recurrences after Cardioversion: A Meta-analysis of Randomized Controlled Trials

“…Long term fish oil supplementation also downregulates profibrillatory cardiac connexins (15) and proinflammatory cytokines implicated in AF perpetuation (21,22). Recently, it was believed that the inflammation played a part in the pathophysiology of atrial remodeling (23). And n-3 fatty acids can attenuate inflammation in humans (24).…”

Simvastatin attenuates sympathetic hyperinnervation to prevent atrial fibrillation during the postmyocardial infarction remodeling process

“…AF has been shown to be closely related to inflammation; however, a direct causative relationship between them has not been established (20). An increasing body of evidence suggests that inflammation can induce autonomic remodeling, resulting in the electrical remodeling for the initiation and maintenance of AF (32).…”

“…A growing body of evidence shows that inflammation and/or oxidative stress play an important role in the pathological process of AF (20); however, the underlying mechanism via which inflammation causes AF is still not well known. Interestingly, in a tachycardiac pacing-induced AF animal model, there shows a significant increase in nerve sprouting and sympathetic hyperinnervation, characterized by a higher density of GAP-43-and tyrosine hydroxylase (TH)-positive staining nerves in the atrium (6,27).…”

Aplastic Anemia and Risk of Incident Atrial Fibrillation ― A Nationwide Cohort Study ―

“…[5][6][7] Several risk factors for AF development have been proposed and among them, inflammation has recently attracted the attention of research. [8][9][10] To the best of our knowledge, there has not been an investigation of an association between AA and the risk of AF development. Hence, the present study sought to use Taiwan insurance data to establish propensity scorematched (PSM) cohorts for evaluating whether patients with AA are at a risk of developing AF, in addition to a comparison with general population controls.…”