This study does not make clear the source of oxidative stress or how oxidative stress is related to AF. As noted above, AF has been associated with cardiac oxidative stress, but a recent trial suggests that oxidative stress in AF may be more widespread. have a role in the development of atrial arrhythmias after cardiac surgery, and that a genetic predisposition to develop postoperative complications exists. Cytokines can have a prognostic significance; IL-6 levels, CRP, UK 356618 and other cytokines may have prognostic value in AF. Cytokine lowering therapies, statins, angiotensin converting enzyme inhibitors and other anti-inflammatory brokers may have a role in the treatment of AF. The present article provides an overview of the evidence linking inflammatory cytokines to AF and their therapeutic and prognostic implications. Keywords:atrial fibrillation, inflammation, cytokines == Introduction == Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. Its prevalence is usually strongly age-dependent, affecting approximately 1% of persons less than 65-years-old, and 5% of individuals aged older than 65 years. AF is also associated with an increase in the relative risk of mortality in both men and women, ranging from 1.3 to 2.3, impartial of other risk factors, as well as an increasing morbidity and adverse affects on quality of life. In particular, patients who present with stroke in AF have a considerably worse outcome, defined by a higher mortality, morbidity, and longer hospital stays compared with patients who have a stroke in the absence of AF.15 There is an increasing body of evidence linking inflammation to a broad spectrum of cardiovascular conditions, such as coronary artery disease (CAD), insulin resistance, diabetes mellitus, and hypertension. In addition, there is emerging data to support an association between inflammation and AF. This has created exciting potential opportunities to target inflammatory processes for the prevention of AF. AF has been associated with myocardial oxidative stress, and antioxidant brokers have demonstrated antiarrhythmic benefit in humans. The structural changes of the atria that define structural remodeling in AF include left atrial dilatation and increasing atrial fibrosis. These structural changes typically occur in parallel with changes of the electrical properties of atrial tissue.6In long-lasting persistent AF, lower levels of interleukin (IL)-6 and C-reactive protein (CRP) appear to be associated with maintenance of sinus rhythm after pharmacological cardioversion irrespective of the use of rennin-angiotensin system (RAS) inhibitors.7Radiofrequency ablation generates a localized myocardial necrosis that might result in a release of inflammatory mediators. Limited studies have investigated this correlation between inflammatory cytokines and AF. Elevated IL-6 and CRP levels in patients with postoperative AF suggest inflammatory components have a role in the pathogenesis of post operative AF.8In addition, higher concentrations of serum IL-8 in coronary artery bypass graft (CABG) patients with postoperative AF suggested a role for inflammation in the pathogenesis of AF after open heart surgery.9Among AF patients, cytokines can have a prognostic significance. The potential for using novel brokers that can influence the inflammatory processes in AF may represent a shift in the way we think of this common arrhythmia, from an electrical to a more structural emphasis.1012Atrial biopsies from patients with AF have confirmed the presence of inflammation. Furthermore, there is preliminary evidence to support the use of a number of drug UK 356618 therapies that have the potential to reduce the clinical burden of AF. On the other hand, conflicting results exist around the activation of tissue cytokines in fibrillating atrial samples.1315The aim of this article is to present an overview of UK 356618 the evidence linking inflammatory cytokines to AF. We reviewed pertinent articles published on Medline, Pubmed, Scopus and EBSCOhostresearch databases till December 2009, using the following indexing terms: inflammation, cytokines, AF, and atrial arrhythmias. == Physiological and immunological perspectives == == Morphological cellular changes in atrial fibrillation == The structural changes of the atria that define structural remodeling in AF include left atrial dilatation and increasing atrial fibrosis. These structural changes typically occur in parallel with changes of the electrical properties of atrial tissue. Key to this fibrotic process is the deposition of increased amounts of connective tissue, including collagen and fibronectin, between individual atrial Rabbit Polyclonal to PWWP2B myocytes. This prospects to separation of myocytes from one another, and subsequent impairment of atrial conduction at the cellular level. All the above result in alterations in the biophysical properties of atrial tissue, allowing the initiation and.