The role of inflammation, fibrosis, and metabolic stress in the formation and maintenance of atrial fibrillation

Atrial fibrillation (AF) is a complex disease with a multifactorial etiology, while the mechanisms of AF associated with inflammation include associated changes in electrophysiological properties, initiation of early and late post-depolarization, remodeling of the heart structure and increased fibrosis. These inflammatory factors cause the appearance of increased ectopic activity and the implementation of the mechanism of re-entry of arousal, which in turn contribute to the initiation and maintenance of AF. It has been established that inflammatory diseases of various etiologies, leading to both systemic and local inflammatory processes, are certainly associated with AF, as evidenced by a distinct increase in the levels of inflammatory markers in this arrhythmia. Fibrosis also plays a significant role in the development of AF, both through electrical and structural atrial remodeling. It promotes increased deposition of extracellular matrix proteins in the myocardial interstitium and creates a structural basis for maintaining the heterogeneity of cardiac tissue. The role of metabolic stress in the pathophysiology of the development and maintenance of AF as a result of the activation of inflammatory processes cannot be ignored. However, inflammation is multifaceted, and different types of inflammation affect the risk of AF in different ways. Moreover, inflammation seems to have a different effect on different AF variants, as well as on its duration. Thus, there is still much to be clarified in the relationship between AF and inflammation. The data reviewed in this article supports the idea that inflammation may be one of the main causes of AF occurrence and maintenance.