Therapeutic Advances in Cardiovascular Disease

 

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Therapeutic Advances in Cardiovascular Disease, Vol. 2, No. 3, 215-223 (2008)
DOI: 10.1177/1753944708092111

Reviews

Review: Atrial fibrillation and renin-angiotensin system

José Luis Serra

Departamento de Arritmias, Sanatorio Allende, Córdoba, Argentina

Mario Bendersky

Department of Pharmacology, Chief Hypertension Unit, Instituto Modelo Cardiología, Córdoba University , Córdoba, Argentina, bendersk{at}inforia.com.ar

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.

Key Words: atrial fibrillation • remodeling • renin-angiotensin system


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