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STATE-OF-THE-ART PAPER

Role of Inflammation in Initiation and Perpetuation of Atrial Fibrillation

A Systematic Review of the Published Data

Division of Cardiology, Baylor College of Medicine, Houston, Texas.

Manuscript received April 30, 2007; revised manuscript received June 13, 2007, accepted June 19, 2007.

^_* Reprint requests and correspondence: Dr. Nasser M. Lakkis, Professor of Medicine, 1709 Dryden, MS 9.90, Houston, Texas 77030. (Email: nlakkis{at}bcm.tmc.edu).

Atrial fibrillation (AF) is the most common arrhythmia in clinical practice. Recent studies have indicated that inflammation might play a significant role in the initiation, maintenance, and perpetuation of AF. Inflammatory markers such as interleukin-6 and C-reactive protein are elevated in AF and correlate to longer duration of AF, success of cardioversion, and thrombogenesis. Furthermore, the inflammatory process might be modulated by the use of statins, angiotensin-converting enzyme inhibitors, or glucocorticoids. The purpose of this study is to analyze the current published reports on the relationship between inflammation and AF and the potential therapeutic options available to modulate the inflammatory milieu in AF.

Abbreviations and Acronyms   ACE = angiotensin-converting enzyme   AERP = atrial effective refractory period   AF = atrial fibrillation   ARB = angiotensin receptor blocker   CABG = cardiac bypass surgery   CRP = C-reactive protein   DCCV = direct current cardioversion   IFN = interferon   IL = interleukin   PAF = paroxysmal atrial fibrillatioin   RAS = renin-angiotensin system   SEC = spontaneous echo contrast   TGF = transforming growth factor   TNF = tumor necrosis factor

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