The Role of Major Inflammatory Biomarkers in the Pathogenesis of Atrial Fibrillation

Many studies have reported a relationship between inflammation and atrial fibrillation (AF). According to the literature, inflammation is the key component in pathophysiological processes during the development of AF; the amplification of inflammatory pathways triggers AF, and, at the same time, AF increases the inflammatory state. The plasma levels of several inflammatory biomarkers are elevated in patients with AF; therefore, inflammation might contribute to both the maintenance and occurrence of AF and its thromboembolic complications. Numerous inflammatory markers have been linked to AF, including CD40 ligand, fibrinogen, matrix metalloproteinase (MMP)-9, monocyte chemoattractant protein-1, myeloperoxidase, plasminogen activator inhibitor-1, and serum amyloid A. There are many pathophysiological aspects of AF that are linked to these inflammatory biomarkers, including atrial structural remodeling and atrial dilatation, increased atrial myocyte expression, fluctuations in calcium cycling, cardiac remodeling promotion, increased cardiac myocyte proliferation and terminal differentiation, production of several MMPs, the pathogenesis of atherosclerosis and cardiomyocyte apoptosis, an increased degree of fibrosis in atrial myocardium, and the progression and development of atherogenesis and atherothrombosis. The present review article aims to provide an updated overview and focus on the basic role of different biomarkers of inflammation in the pathophysiological aspects of the pathogenesis of AF.