Atrial Fibrillation (AF) is one of the most frequent arrhythmias, especially in elderly patients. Cardiac overload increases the incidence of AF. Clinical presentation of atrial fibrillation can occur as nonsustained paroxysms, persistent episodes and in chronic-permanent form. The physio-pathological mechanisms are:• Circuit of multiple and anarchic re-entries • Atrial fibrillatory conduction • Re-entry circuit with fibrillatory conduction. Remodeling (electrical or structural) facilitates the appearance and persistence of AF: Neurovegetative changes and cytosolic Ca overload facilitate AF. Interstitial atrial fibrosis, in which Renin-Angiotensin System (RAS) hyperactivity is a main aspect of remodeling. There is clinical evidence that supports the antiatrial fibrillatory actions of RAS blockade. Potential mechanisms are: (a) direct modulation of ionic channels, (b) hemodynamic improvement, (c) reduction of atrial stretching, (d) antifibrotic effects. There is less clinical evidence with antialdosterone drugs, but theoretically these might also be useful.
Keywords: atrial fibrillation, remodeling, renin-angiotensin systemAtrial fibrillation, pathophysiology, remodeling. Atrial fibrillation (AF) is one of the most frequent arrhythmias in adulthood, with its incidence increasing with age. The situations and pathologies that lead to hemodynamic or pressure overload are associated to AF. This can be present as nonsustained paroxysms, persistent episodes (reverted to Sinus Rhythm by medical treatments) and as chronic-permanent AF. It is referred to as 'isolated' when there is no structural cardiopathy or other morbid entities that can explain it. Three mechanisms have been described to explain its physiopathogenia [Nattel and Ehrlich, 2004]: a. Multiple, coexistent, anarchic re-entry circuits. AF settles down if the conditions are appropriate for them to appear and persist over time. These alterations involve refractoriness (reduction), velocity of conduction (delay), and an increase in heterogeneity of both properties [Moe and Abildskov, 1995;Cosio, 1994;Cosio and Arribas, 1989;Allessie, et al. 1985;Moe, 1962]. The quantity of atrial 'mass' (atrial volume) is also a determining factor. For hearts with big atria, AF is more frequent and lasting [Henry et al. 1976]. The persistence of the fibrillatory state depends on the number of the aforementioned re-entries circuits that are simultaneously present, at any determined moment. Few coexistent re-entries diminish the possibility of persistence.b. Rapid and continued ectopic activity, with 'fibrillatory conduction' in auricles, due to its impossibility to respond in an organized form.c. Only one circuit of re-entry with 'fibrillatory conduction,' with this 'fibrillatory conduction' also depending on the heterogeneity of refractoriness and atrial conductivity.An interrelationship may exist between these three mechanisms.An episode of AF needs a 'trigger' (premature beats, tachycardia) to initiate it, by interaction with 'modulators' (neurovegetative system, br...