Long-standing atrial fibrillation is associated with significant morbidity including stroke and development of heart failure. Patients also report poor quality of life as a result of debilitating symptoms or treatment side effects from antiarrhythmic medications. Radio frequency or cryothermal mediated catheter ablation has a central role in the management of symptomatic patients with paroxysmal or persistent atrial fibrillation. Circumferential pulmonary vein isolation is vital to the success of this therapy and other ancillary techniques have been described, especially for persistent atrial fibrillation. Several randomized controlled studies have been reported over the last two decades studying important clinical outcomes in patients with atrial fibrillation. In this article, we aim to provide a review of the major studies that have helped define the role of catheter ablation in the management of symptomatic atrial fibrillation in patients with both diseased and structurally normal hearts.Atrial fibrillation is a common arrhythmia which may cause symptoms that significantly impact quality of life and is associated with increased risk of stroke, heart failure, and sudden death. Over the past three decades many surgical techniques as well as catheter-bases procedures have been developed to treat atrial fibrillation. In this review we describe the indications, treatments, outcomes, surgical techniques, and technical advances reported in the literature.Atrial fibrillation is the most common arrhythmia in the adult population, and its incidence and prevalence are still rising. Cardiac devices are widely used in clinical practice in the management of various rhythm disturbances and heart failure treatment. Many patients who receive a pacemaker, implantable cardioverter-defibrillator, or cardiac resynchronization therapy also experience atrial fibrillation in the course of their life. Therefore, this review aims to describe the role of these devices in the treatment and prevention of atrial fibrillation in the device recipients. In addition, all these implantable devices also serve as permanent ECG (electrocardiogram) monitors, thus providing important information about the presence and characteristics of atrial fibrillation that may or may not be detected by the patient but can modify our therapeutical approach with regard to the stroke prevention.Atrial fibrillation (AF) is a rhythm disturbance defined by irregular, rapid electrical, and mechanical activation of the atria, which causes unsynchronized atrial contraction and promotes thromboembolism. AF is the most common sustained arrhythmia. Its prevalence and incidence are increasing due to aging and improved survival from acute heart diseases. This article is a review on AF management from both a surgical and catheter-based perspective. While both treatment approaches to AF have been shown to be successful in the management of AF, they are not without their own inherent complications. This article seeks to review some of these complications and help to guide treatment.In atrial fibrillation (AF), oral anticoagulant (OAC) therapy with either vitamin K antagonist or non-vitamin K antagonist is used to prevent thromboembolic complications. In patients who presented with acute coronary syndrome (ACS) and were treated by percutaneous coronary intervention (PCI), dual antiplatelet therapy (DAPT) with aspirin and a P2Y 12 inhibitor reduces major adverse cardiac events (MACEs) and stent thrombosis. Consequently, in patients with AF who presented with ACS and were treated by PCI, the combination of OAC and DAPT, the so-called triple antithrombotic therapy (TAT) is needed to improve the outcome of the patients. However, the use of TAT increases the risk of bleeding. Several randomized clinical trials and a meta-analysis evaluated the use of TAT and double antithrombotic therapy (DAT) in this population, and DAT is defined as patients who receive combination of one antiplatelet and OAC. In general, the studies demonstrated a reduction in bleeding event in patients who received DAT as compared with TAT, with similar incidence of thromboembolic complications and MACE. To date, there is no established consensus or guideline for the most appropriate combination of antithrombotic agents in patients with AF and ACS who undergo PCI. Tailoring the treatment for each individual is likely the best approach to determine the balance of bleeding risk and ischemic events before starting antithrombotic therapy. Future trials with adequate sample size are needed to find the most appropriate combination of antiplatelet and OAC in patients with AF who presented with ACS and treated by PCI.Atrial fibrillation (AF) is the most common of cardiac arrhythmias. Mechanisms such as atrial structural remodeling and electrical remodeling have been implicated in the pathogenesis of AF. The data to date suggest that advanced glycation end products (AGEs) and its cell receptor RAGE (receptor for AGE) and soluble receptor (sRAGE) are involved in the pathogenesis of AF. This review focuses on the role of AGE-RAGE axis in the pathogenesis of AF. Interaction of AGE with RAGE generates reactive oxygen species, cytokines, and vascular cell adhesion molecules. selleck kinase inhibitor sRAGE is a cytoprotective agent. The data show that serum levels of AGE and sRAGE, and expression of RAGE, are elevated in AF patients. Elevated levels of sRAGE did not protect the development of AF. This might be due to greater elevation of AGE than sRAGE. Measurement of AGE-RAGE stress (AGE/sRAGE) would be appropriate as compared with measurement of AGE or RAGE or sRAGE alone in AF patients. AGE and its interaction with RAGE can induce AF through alteration in cellular protein and extracellular matrix. AGE and its interaction with RAGE induce atrial structural and electrical remodeling. The treatment strategy should be directed toward reduction in AGE levels, suppression of RAGE expression, blocking of binding of AGE to RAGE, and elevation of sRAGE and antioxidants. In conclusion, AGE-RAGE axis is involved in the development of AF through atrial structural and electrical remodeling. The treatment modalities for AF should include lowering of AGE, suppression of RAGE, elevation of sRAGE, and use of antioxidants.