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1.  Inflammatory cytokines and atrial fibrillation: current and prospective views 
Atrial fibrillation (AF) is the most common sustained arrhythmia and a challenging clinical problem encountered in daily clinical practice. There is an increasing body of evidence linking inflammation to a broad spectrum of cardiovascular conditions including AF. Historical evidence supports an association between AF and inflammation and is consistent with the association of AF with inflammatory conditions of the heart, such as myocarditis and pericarditis. AF has been associated with myocardial oxidative stress, and antioxidant agents have demonstrated antiarrhythmic benefit in humans. Increased plasma interleukin (IL)-6, C-reactive protein (CRP), and plasma viscosity support the existence of an inflammatory state among “typical” populations with chronic AF. These indexes of inflammation are related to the prothrombotic state and may be linked to the clinical characteristics of the patients (underlying vascular disease and comorbidities), rather than simply to the presence of AF itself. It has been suggested that inflammation may 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, and other cytokines may have prognostic value in AF. Cytokine lowering therapies, statins, angiotensin converting enzyme inhibitors and other anti-inflammatory agents 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.
doi:10.2147/JIR.S10095
PMCID: PMC3218735  PMID: 22096359
atrial fibrillation; inflammation; cytokines
2.  Pleiotropic effects of statins in atrial fibrillation patients: the evidence 
Atrial fibrillation (AF) is the most common sustained arrhythmia in clinical practice. The understanding of the pathophysiology of AF has changed during the last several decades, and a significant role of inflammation and of the renin–angiotensin–aldosterone system has been postulated both experimentally and clinically. There is emerging evidence of an association between inflammation and AF, and mounting evidence links increased C-reactive protein levels not only to already existing AF but also to the risk of developing future AF. The beneficial effects of statins on AF have been reported in several studies. Several randomized clinical and large observational studies have shown similar result that show the beneficial effect of statins in AF. In clinical studies, statins were considered effective in preventing AF after electrical cardioversion, post-ablation, and after permanent pacemaker and implantable cardioverter defibrillator insertion. The antiarrhythmic mechanisms of statins regarding AF prevention in patients with heart failure are still not clear. Perioperative statin use has been associated with favorable postoperative outcome in both cardiovascular and noncardiovascular conditions. Despite a growing body of evidence that drugs with anti-inflammatory properties such as statins may prevent AF, the observed positive effects of statins on the burden of AF appeared to be independent of their cholesterol-reducing properties. However, further data from large-scale randomized trials are clearly needed.
PMCID: PMC2704895  PMID: 19590588
statins; pleiotropic effects; atrial fibrillation
3.  Endothelial dysfunction in diabetes mellitus 
Diabetes mellitus is associated with an increased risk of cardiovascular disease, even in the presence of intensive glycemic control. Substantial clinical and experimental evidence suggest that both diabetes and insulin resistance cause a combination of endothelial dysfunctions, which may diminish the anti-atherogenic role of the vascular endothelium. Both insulin resistance and endothelial dysfunction appear to precede the development of overt hyperglycemia in patients with type 2 diabetes. Therefore, in patients with diabetes or insulin resistance, endothelial dysfunction may be a critical early target for preventing atherosclerosis and cardiovascular disease. Microalbuminuria is now considered to be an atherosclerotic risk factor and predicts future cardiovascular disease risk in diabetic patients, in elderly patients, as well as in the general population. It has been implicated as an independent risk factor for cardiovascular disease and premature cardiovascular mortality for patients with type 1 and type 2 diabetes mellitus, as well as for patients with essential hypertension. A complete biochemical understanding of the mechanisms by which hyperglycemia causes vascular functional and structural changes associated with the diabetic milieu still eludes us. In recent years, the numerous biochemical and metabolic pathways postulated to have a causal role in the pathogenesis of diabetic vascular disease have been distilled into several unifying hypotheses. The role of chronic hyperglycemia in the development of diabetic microvascular complications and in neuropathy has been clearly established. However, the biochemical or cellular links between elevated blood glucose levels, and the vascular lesions remain incompletely understood. A number of trials have demonstrated that statins therapy as well as angiotensin converting enzyme inhibitors is associated with improvements in endothelial function in diabetes. Although antioxidants provide short-term improvement of endothelial function in humans, all studies of the effectiveness of preventive antioxidant therapy have been disappointing. Control of hyperglycemia thus remains the best way to improve endothelial function and to prevent atherosclerosis and other cardiovascular complications of diabetes. In the present review we provide the up to date details on this subject.
PMCID: PMC2350146  PMID: 18200806
endothelial dysfunction; diabetes mellitus; hyperglycemia; insulin resistance microalbumiuria
4.  Endothelial Dysfunction: Cardiovascular Risk Factors, Therapy, and Outcome 
Endothelial dysfunction is a well established response to cardiovascular risk factors and precedes the development of atherosclerosis. Endothelial dysfunction is involved in lesion formation by the promotion of both the early and late mechanisms of atherosclerosis including up-regulation of adhesion molecules, increased chemokine secretion and leukocyte adherence, increased cell permeability, enhanced low-density lipoprotein oxidation, platelet activation, cytokine elaboration, and vascular smooth muscle cell proliferation and migration. Endothelial dysfunction is a term that covers diminished production/availability of nitric oxide and/or an imbalance in the relative contribution of endothelium-derived relaxing and contracting factors. Also, when cardiovascular risk factors are treated the endothelial dysfunction is reversed and it is an independent predictor of cardiac events. We review the literature concerning endothelial dysfunction in regard to its pathogenesis, treatment, and outcome.
PMCID: PMC1993955  PMID: 17319104
endothelial dysfunction; coronary atherosclerosis; coronary artery disease

Results 1-4 (4)