PATHOPHYSIOLOGICAL AND STRUCTURAL PECULIARITIES OF CARDIAC FIBROSIS DEVELOPMENT IN ATRIAL FIBRILLATION

Introduction. In recent years, the study of the pathogenesis of atrial fibrillation (AF) and its complications resulting from this condition has drawn substantial attention from cardiologists. A comprehensive understanding of this issue is essential for investigating the structural and functional disturbances occurring in the heart during AF. These data are also important for developing novel therapies aimed at preventing the onset and progression of cardiac fibrosis. The aim of this study is to identify the primary pathways that activate cardiac connective tissue cells involved in fibrosogenesis, to examine the structural characteristics of this pathological process, and to investigate the role of fibroblasts in initiating and progressing cardiac fibrosis. Materials and Methods. The primary data for this article were collected through an in-depth analysis of recent scientific literature, with a focus on studies published in the last 5–7 years. Results. A detailed review of primary sources reveals that this cardiological issue has only been partially explored. Findings indicate a close link between the pathophysiological and structural mechanisms of AF and numerous resulting complications, with cardiac fibrosis being a primary consequence. Two major forms of fibrous damage to atrial cardiomyocytes play a key role in the development of cardiac fibrosis associated with AF. This includes both reactive and reparative types of cardiac fibrosis, which develop concurrently in atrial fibrillation. These structural changes lead not only to damage and loss of cardiomyocytes but also to pathological remodeling of fibroblasts, the intercellular matrix, and the atria and ventricles. Disruptions in bioelectrical potential conduction are also observed. Activated fibroblasts play a central role in initiating cardiac fibrosis, with key stages of protein synthesis involved in atrial fibrosis now better understood. Specific intracellular signaling pathways, which present potential therapeutic targets for preventing cardiac fibrosis in AF treatment, have been identified. Conclusion. Atrial fibrillation and cardiac fibrosis are interdependent, with each potentially accelerating the progression of the other. These pathological processes are underpinned by significant structural and functional disruptions within cardiac cells and the intercellular matrix. Fibroblasts, myofibroblasts, and intensive fibrous tissue formation within the matrix are pivotal in the development of cardiac fibrosis. A preventive strategy targeting early intervention in cardiac fibrosis shows the greatest therapeutic promise.