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Furthermore, rhythm control using catheter ablation is an emerging treatment option for AF. Catheter ablation is more efficient at reducing the AF burden compared with antiarrhythmic drugs (AADs). However, Trichostatin A the effectiveness of catheter ablation at reducing the risks of mortality and stroke is not yet evident. The current American Heart Association, American College of Cardiology, and Heart Rhythm Society guidelines suggest that catheter ablation for AF should not be performed on patients who cannot be treated with OAC therapy during and after the procedure. Catheter ablation for AF to restore sinus rhythm should not be performed with the sole intent of obviating the need for OAC therapy. There is insufficient evidence available to determine whether catheter ablation for AF reduces all-cause mortality, stroke, and heart failure. Thromboembolic events in the control arm of the RAte Control versus Electrical cardioversion study were more common in the patients who had stopped OAC therapy or had unsatisfactory international normalized ratios [14]. Similarly, most of the patients who experienced strokes in the Atrial Fibrillation Follow-Up Investigation of Rhythm Management study were not receiving warfarin or they had suboptimal international normalized ratios at the times of their strokes [15]. Clearly, the premature cessation of OAC therapy in one-third of the rhythm-controlled patients in the Atrial Fibrillation Follow-Up Investigation Casein kinase 2 of Rhythm Vismodegib in vivo Management trial rendered them vulnerable to thromboembolic consequences. The strategy underlying AF treatment to reduce the risk of stroke is evolving, especially in the era of novel OAC therapies. Atrial fibrillation and cryptogenic stroke AF is a major independent predictor of ischemic stroke. The estimated risk of AF during a lifetime is between 22% and 26% [16]. AF is associated with abnormal blood stasis that involves atrial hypocontractility and the loss of the atrial kick, atrial structural remodeling, and the activation of platelets and the coagulation cascade, which is known as Virchow��s triad. In addition, AF provides a prothrombotic environment through atrial dilation and stretching, a reduction in the pectinate muscle volume, the loss of a normal endocardial surface, endothelial dysfunction, and the release of coagulation factors, namely, factor Xa and thrombin. These AF characteristics promote thrombus formation and ischemic stroke. AF is a significant underlying cause of cardiac emboli in approximately 50% of patients. Stroke of an unknown cause is more frequent in younger patients. Cryptogenic stroke causes up to 40% of the strokes in patients who are
