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Current Medicinal Chemistry

Editor-in-Chief

ISSN (Print): 0929-8673
ISSN (Online): 1875-533X

Renin-Angiotensin System Block and Atrial Fibrillation

Author(s): Federico Lombardi and Paolo Terranova

Volume 12 , Issue 11 , 2005

Page: [1331 - 1337] Pages: 7

DOI: 10.2174/0929867054020954

Price: $65

Abstract

Atrial fibrillation is the most common disorder of cardiac rhythm. In spite of diagnosis simplicity, patients with atrial fibrillation are difficult to treat. In the recent years with the description of the phenomenon called remodelling, it has been possible to better define the principle mechanisms responsible for initiation, maintenance and, in some instances, termination of atrial fibrillation. Electrical, mechanical and anatomical remodelling indicate those alterations that, once established, may vanish any attempt to restore sinus rhythm. Atrial fibrosis is probably the most critical component of the remodelling process and appears to be largely mediated by the activation of the Renin-Angiotensin-Aldosterone System. Both experimental and clinical data have confirmed the pro-arrhythmic role of the Renin-Angiotensin-Aldosterone System and demonstrated an anti-arrhythmic effects of ACE-inhibitors and AT1 receptor blockers. Regarding atrial fibrillation, it has been recently reported that the adjunction of AT1 receptor blocker to amiodarone was more effective than the antiarrhythmic drug alone, in reducing arrhythmia recurrence after electrical cardioversion. This and subsequent clinical observations indicate that pharmacological interventions capable of interfering with the electrical and structural remodelling process are of critical importance in the management of patients with atrial fibrillation. ACE inhibitors and AT1 receptor blockers represent new and efficient therapeutical options to contrast the nearly inevitable progression of this arrhythmia towards its permanent form.

Keywords: ace inhibitors, atrial fibrillation, structural remodelling, heart failure, pharmacological treatment, anti-arrhythmic drugs, at receptor blockers


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