Fibrosis is one of the most studied mechanisms of development of atrial fibrillation (AF). This mechanism is supported by electrical and structural remodeling of the atria. In recent years, oxidative stress has also been investigated as a potentially important mechanism for the development of AF. Reactive oxygen species are products formed as a result of oxygen metabolism. It has been proven that these molecules have a multifaceted effect on the cells present in the heart tissue. In addition, inflammation contributes to atrial remodeling, which includes both structural and electrophysiological changes that form the basis of the disease. Linking inflammation with the occurrence of AF, it is important to mention the role of coronary heart disease. Coronary heart disease has been associated with the development of AF through various mechanisms. After myocardial ischemia, both local and systemic inflammation occurs, which causes the release of various inflammatory factors, such as IL-6 and C-reactive protein. As is known, systemic inflammation has a prothrombotic effect, which in combination with AF increases the risk of thromboembolic events. Thus, this article presents the modern view of a cardiologist on the pathophysiological causes of the development and maintenance of AF.