Abstract

Atrial fibrillation (AF) is the most common arrhythmia and one of the major causes of morbidity and hospitalization. It is an important risk factor for thromboembolic complications and cerebrovascular disease. In AF, extensive electrical and structural remodeling of atrial tissue takes place with the main underlying mechanisms being inflammation and fibrosis. In recent years it has been shown, that beside conventional antiarrhythmic therapies, modalities aiming at reversal of atrial tissue derangement could be of some benefit in the treatment of AF. In this respect, the main focus was oriented towards drugs such as angiotensin convertase (ACE) inhibitors, angiotensin receptor blockers (ARBs), polyunsaturated fatty acids and statins. Data about the potential beneficial role of statins for AF treatment is continuously growing. It is now evident that statins act on AF mainly through their pleiotropic and not their lipid lowering properties. Several retrospective trials have shown that statins exert antiarrhythmic effects in patients with AF, while data from prospective studies are still conflicting. Thus, the definitive confirmation and explanation of statin's role in AF treatment is still missing. Herein, the current patophysiological concepts providing rationale for the use of statins in AF treatment as well as up-to-date data from retrospective and prospective clinical studies are reviewed and discussed. Particular attention is paid to various clinical settings such as primary prevention, secondary prevention (post-cardioversion) and postoperative setting. We also present our own data regarding the role of statins in prevention of the recurrence of AF after successful cardioversion.

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