Role of Inflammation in Initiation and Perpetuation of Atrial Fibrillation : A Systematic Review of the Published Data

• Published in: Journal of the American College of Cardiology Vol. 50; no. 21; pp. 2021 - 2028
• Main Authors: ISSAC, Tim T, DOKAINISH, Hisham, LAKKIS, Nasser M
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Science 20-11-2007; Elsevier Limited
• Subjects: Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Animals; Atrial Fibrillation - blood; Atrial Fibrillation - etiology; Atrial Fibrillation - physiopathology; Biological and medical sciences; Biomarkers - blood; C-Reactive Protein - analysis; Cardiac arrhythmia; Cardiac dysrhythmias; Cardiology; Cardiology. Vascular system; Cardiovascular disease; Clinical Trials as Topic; Cytokines; Drug therapy; Enzymes; Glucocorticoids - therapeutic use; Heart; Heart attacks; Heart failure; Heart surgery; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Inflammation - blood; Inflammation - complications; Interleukin-6 - blood; Medical sciences; Mortality; Older people; Proteins; Studies; Thrombosis - physiopathology; Arrhythmia; Heart disease; Atrial fibrillation; Cardiovascular disease; Systematic review; Inflammation; Circulatory system; Cardiology; Initiation; Excitability disorder
• ISSN: 0735-1097; 1558-3597
• DOI: 10.1016/j.jacc.2007.06.054

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.