European Heart Journal Advance Access originally published online on June 23, 2005
European Heart Journal 2005 26(20):2083-2092; doi:10.1093/eurheartj/ehi350
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Inflammation in the genesis and perpetuation of atrial fibrillation
Department of Cardiology 2142, The Heart Center, University Hospital of Copenhagen, Rigshospitalet, Blegdamsvej 9, DK-2100 Copenhagen O, Denmark
Received 13 December 2004; revised 12 April 2005; accepted 11 May 2005; online publish-ahead-of-print 23 June 2005.
* Corresponding author. Tel: +45 43 45 38 48; fax: +45 43 45 38 24. E-mail address: engelmann{at}dadlnet.dk
The prevalence and persistence of atrial fibrillation (AF) and the relative inefficacy of the currently available pharmacotherapy requires development of new treatment strategies. Recent findings have suggested a mechanistic link between inflammatory processes and the development of AF. Epidemiological studies have shown an association between C-reactive protein and both the presence of AF and the risk of developing future AF. In casecontrol studies, C-reactive protein is significantly elevated in AF patients and is associated with successful cardioversion. Moreover, C-reactive protein elevation is more pronounced in patients with persistent AF than in those with paroxysmal AF. Furthermore, treatment with glucocorticoids, statins, angiotensin converting enzyme inhibitors, and angiotensin II receptor blockers seems to reduce recurrence of AF. Part of this anti-arrhythmic effect may be through anti-inflammatory activity. This article reviews what is known about inflammation in genesis and perpetuation of AF, the putative underlying mechanisms, and possible therapeutic implications for the inhibition of inflammation as an evolving treatment modality for AF.
Key Words: Atrial fibrillation Inflammation C-reactive protein Glucocorticoid Statin
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