Atrial fibrillation and the renin-angiotensin-aldosterone system

Perlini, Stefano
Chang, Edward S.
Mayer, Tim E.
Salinaro, Francesco

¹ Clinica Medica II, Department of Internal Medicine, Fondazione IRCCS San Matteo, University of Pavia, Pavia, Italy
² Division of Cardiology, Radcliffe Hospital, Oxford, UK
³ Division of Cardiology, University of Cincinnati Medical Center, Cincinnati, Ohio, USA

Correspondence: Professor Stefano Perlini, Dipartimento di Medicina Interna, Università di Pavia, P. le Golgi 19, 27100 Pavia, Italy.

E-mail: [email protected]

Cardiology & Clinical Practice - La Cardiologia nella Pratica Clinica 3(2):p 85-89, May 1, 2011. | DOI: 10.2165/11592330-000000000-00000

Atrial fibrillation (AF) is the most common chronic cardiac arrhythmia and a major public health problem, leading to high rates of morbidity and mortality. The onset of AF results from a complex interaction between triggers, arrhythmogenic substrate and modulator factors. Once established, AF itself alters the electrical and structural properties of the atrial myocardium, thereby perpetuating the arrhythmia. Among many other factors, angiotensin II plays an important role not only in contributing to the development of atrial fibrosis, but also in modulating the electrical properties of the atrial myocardium. These aspects may be relevant in explaining the many clinical observations indicating the role of drugs modulating the renin-angiotensin-aldosterone system in preventing AF in different settings.