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 anti-arrhythmic 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. (copyright) 2005 Bentham Science Publishers Ltd.

Renin-angiotensin system block and atrial fibrillation / P. Terranova, F. Lombardi. - In: CURRENT MEDICINAL CHEMISTRY. - ISSN 0929-8673. - 12:11(2005), pp. 1331-1337.

Renin-angiotensin system block and atrial fibrillation

F. Lombardi
Ultimo
2005

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 anti-arrhythmic 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. (copyright) 2005 Bentham Science Publishers Ltd.
antiarrhythmic activity; antiinflammatory activity; cardioversion; clinical observation; clinical trial; drug efficacy; drug mechanism; evidence based medicine; heart arrhythmia; heart atrium fibrillation; heart electrophysiology; heart muscle fibrosis; heart proarrhythmia; heart ventricle remodeling; human; meta analysis; pathogenesis; recurrent disease; renin angiotensin aldosterone system; review; sinus rhythm; C reactive protein; amiodarone; angiotensin 1 receptor antagonist; antiarrhythmic agent; anticoagulant agent; calcium channel blocking agent; candesartan; dipeptidyl carboxypeptidase inhibitor; enalapril; hydroxymethylglutaryl coenzyme A reductase inhibitor; irbesartan; long acting drug; losartan; methylprednisolone; placebo; trandolaprilat; valsartan
Settore MED/11 - Malattie dell'Apparato Cardiovascolare
2005
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/5136
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