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J Am Coll Cardiol, 2007; 50:2021-2028, doi:10.1016/j.jacc.2007.06.054 (Published online 5 November 2007).
© 2007 by the American College of Cardiology Foundation
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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

Tim T. Issac, MD, Hisham Dokainish, MD, FACC and Nasser M. Lakkis, MD, FACC*

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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