Review: Atrial fibrillation and renin-angiotensin system

Abstract

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...

Effect of Telmisartan on Paroxysmal Atrial Fibrillation Recurrence in Hypertensive Patients With Normal or Increased Left Atrial Size

“…8 -11 Angiotensin II (Ang II) has been demonstrated to play a pivotal role in atrial remodeling by promoting atrial myocyte hypertrophy and fibrosis. 12,13 Ang II also exerts direct proarrhythmic effects in human atrial myocardium by modifying ion exchanges within atrial cells. 14 Furthermore, Ang II has proinflammatory and prothrombotic properties that might contribute to a prothrombotic status in AF.…”

Effect of Telmisartan and Ramipril on Atrial Fibrillation Recurrence and Severity in Hypertensive Patients With Metabolic Syndrome and Recurrent Symptomatic Paroxysmal and Persistent Atrial Fibrillation

“…[11][12][13][14] Activation of the renin-angiotensin system (RAS), which coexists with both hypertension and metabolic syndrome, is also thought to be involved in the pathophysiology of AF. [15][16][17] Angiotensin II is known to modulate cardiac ionic currents and sympathetic tone and to stimulate fibroblast proliferation and cardiomyocte apoptosis. [15][16][17] Furthermore, there is evidence for a role of angiotensin II (Ang II) in mediating inflammatory responses, which are additionally involved in AF.…”

“…[15][16][17] Angiotensin II is known to modulate cardiac ionic currents and sympathetic tone and to stimulate fibroblast proliferation and cardiomyocte apoptosis. [15][16][17] Furthermore, there is evidence for a role of angiotensin II (Ang II) in mediating inflammatory responses, which are additionally involved in AF. 9,10 Genetic variation in the RAS and altered expression of Ang II receptors are also associated with AF, further indicating an important role in AF.…”

Effect of ramipril/hydrochlorothiazide and ramipril/canrenone combination on atrial fibrillation recurrence in hypertensive type 2 diabetic patients with and without cardiac autonomic neuropathy

“…Subjects with diabetes frequently suffer from cardiac autonomic neuropathy (CAN) [4, 5], which may contribute to creation of electrical instability leading to AF [2]. The renin-angiotensin-aldosterone system (RAAS) is well known to play a major role in the pathophysiology of AF, being involved in myocardial fibrosis, oxidative stress, inflammation and electrical abnormalities, which all contribute to the atrial remodeling underlying the occurrence of this arrhythmia [6]. As a consequence, RAAS blockade has been shown to be effective in preventing new onset as well as recurrence of AF in a variety of clinical settings [7].…”