Abstract
This study analyzed and demonstrated the role of inflammatory mechanisms and inflammation markers in the development of atrial fibrillation, their significance in the structural and electrical remodeling of the atria, and pharmacological agents that can be effective in reducing inflammation. Data were obtained from the analysis of retrospective and prospective studies and systematic reviews. The available domestic and foreign scientific studies indexed in PubMed, Google Scholar, and eLibrary.ru were analyzed. Atrial fibrillation is one of the most common arrhythmias in adults and is associated with many complications and mortality. The pathophysiological mechanisms of this arrhythmia remain completely unclear, and their search continues at the molecular level. Atrial fibrillation causes electrical and structural changes in the myocardium, which lead to further pathological transformations of the heart, and some of them are associated with inflammation, which has been demonstrated in studies on an experimental model and heart tissues of patients with this rhythm disorder. Whether inflammation is the cause of the development of this arrhythmia or its consequence is not clearly understood. Statins, corticosteroids, colchicine, genetically engineered biological drugs, which have a specific application point in the inflammatory cascade, and some other drugs, such as anticoagulants, polyunsaturated fatty acids, angiotensin-converting enzyme inhibitors, angiotensin receptor blockers, and mineralocorticoid receptor antagonists, also take place in the treatment of atrial fibrillation. However, their applications are not clearly specified. Currently, research continuously aims at finding effective ways to prevent and treat this nosology. Thus, promising ways to reduce the role of inflammation in the occurrence, recurrence, diagnosis, and treatment of atrial fibrillation are relevant in the development of precision medicine.