الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
AF is the most common sustained cardiac arrhythmia, occurring in 1–2% of the general population, increasing with age. Cross-sectional studies have found a lower prevalence in those below the age of 60 y, increasing to 8% in those older than 80 y. AF may be related to heart Diseases such as CAD, HF, valvular heart disease, hypertension, congenital heart disease, cardiomyopathies or it may be related to reversible causes such as surgery, MI, pericarditis, myocarditis, pulmonary embolism, alcohol intake, hyperthyroidism, and other metabolic disorders. Patient with AF may suffer from palpitations, fatigue, lightheadedness, and exertional dyspnea, Polyuria, embolic complication and syncope. AF confers a 5-fold risk of stroke, and one in five of all strokes is attributed to this arrhythmia. Ischaemic strokes in association with AF are often fatal, and those patients who survive are left more disabled by their stroke and more likely to suffer a recurrence than patients with other causes of stroke. AF is a complex disease with multiple possible mechanisms which requires a trigger for initiation and a substrate for maintenance. Many studies have proved the arrhythmogenic mechanisms of the PVs as an AF initiator; the mechanisms include enhanced automaticity, triggered activity, and microreentry from myocardial sleeves inside PVs. Once initiated, AF alters atrial electrical and structural properties (atrial remodeling) in a way that promotes its own maintenance and recurrences and may alter the response to antiarrhythmic drugs (AF begets AF). In addition to anticoagulant therapy, there are two main treatment strategies for AF: rhythm control and rate control. Rhythm control aims to revert AF to normal sinus rhythm using electrical direct-current defibrillation, anti-arrhythmic drugs, or a combination of both. Rate control focuses on controlling the ventricular rate while leaving the heart in AF rhythm by using rate slowing medication. Both strategies have limitations. Rate control medications carry some risk of excessive slowing of heart rate. Not all attempts at attaining rhythm control are successful, and drugs to control rhythm may precipitate new or more frequent arrhythmias. There are several new pharmacological agents for the management of AF and many others that are currently under clinical investigation. New anti-arrhythmic drugs targeting multiple channels or having a specific high affinity to the atrial myocardium are believed to have a more favourable risk–benefit ratio than traditional anti-arrhythmic drugs. new therapies, such as atrial repolarization-delaying agents, gap junction modulators and effective upstream therapy with ACE inhibitors, ARBs, statins, omega-3 polyunsaturated fatty acids , anti-inflammatory and anti-fibrotic therapy, may offer a much more comprehensive and effective anti- arrhythmic strategy than is currently available. Like medical therapy for AF, catheter ablation for AF can be divided into two general strategies: rate control and rhythm control. Within the field of catheter ablation, rate can be controlled through modifying the AV node or ablating the node and implanting a permanent pacemaker. Curative catheter ablation achieves rhythm control through targeting the triggers of atrial fibrillation, restoring sinus rhythm, and preventing future recurrences. The role of devices in AF therapy has evolved from conventional bradycardia pacing in sick sinus syndrome and for patients with a slow ventricular response in chronic AF or following AV junctional ablation to atrial pacing for AF prevention and antitachycardia pacing or atrial defibrillation for AF termination. The future holds a lot in store as regards pharmacologic and nonpharmacologic therapies as more advanced molecular biology, imaging, and mapping techniques evolve. Someday, we may finally be ideally equipped to deal with AF, and, eventually, the simple yet complete cure may be in sight.