Atrial fibrillation (AF) represents the most common arrhythmia encountered in clinical practice. The pathophysiology of AF is complex, but in most cases it may be caused by multiple random re-entering wavelets. As generally known, the development of AF leads to electrophysiological and cellular changes in the atria that tend to sustain AF, a process known as electrical remodeling. In addition, it has been proposed that electrical remodeling contributes to the high incidence of early recurrence of AF after cardioversion. The principal characteristics of this process are the shortening of the refractory period with increased dispersion, the loss of rate adaptation, and the reduction of atrial conductivity. On the molecular level, calcium accumulation in myocytes seems to trigger electrophysiological changes leading to reduction in the intensity of L-type calcium current. Currently, the role of inflammation and oxidative stress on electrical remodeling is under investigation. C-reactive protein (CRP), a major inflammatory marker, has been found to be increased in both persistent and paroxysmal AF. Additionally, CRP may have prognostic significance regarding successful cardioversion of AF, and may predict recurrences of arrhythmia. On the other hand, it has been demonstrated that increased oxidative damage occurs in the atria of AF patients and may contribute to electrical remodeling. Interestingly, a prodromal antioxidant intervention study showed beneficial effects from vitamin C on incidence of postoperative AF. The role of inflammation and oxidative stress in AF deserves further study, since amelioration of atrial electrical remodeling by conventional antiarrhythmics has been proved ineffective.

Keywords: Inflammation - physiopathology