Abstract
**Cardioembolism** is the underlying cause in approximately 20% of ischemic stroke cases. Atrial fibrillation (AF) is the most common source of cardioembolic stroke. Stroke due to AF is typically associated with higher rates of mortality and disability compared to strokes of other etiologies, and also carries a higher rate of recurrence. For these reasons, primary and secondary stroke prevention is of critical importance in patients with atrial fibrillation. Data from clinical trials as well as meta-analyses have demonstrated that vitamin K antagonists (VKAs) are an effective means of stroke prevention in patients with atrial fibrillation. In contrast, antiplatelet agents do not provide meaningful preventive efficacy against AF-related stroke and are therefore not recommended for use in this patient population. The use of vitamin K antagonists is fairly complex due to their narrow therapeutic window, requiring frequent INR monitoring and dose adjustments to maintain an INR of 2–3. In addition to this inconvenience, concern over hemorrhagic complications associated with VKA use is a major reason why the proportion of AF patients receiving vitamin K antagonist therapy remains relatively low. Non-vitamin K antagonist oral anticoagulants (NOACs) have been shown to be equally or more effective, as well as safer, than vitamin K antagonists. NOACs also offer the convenience of fixed dosing without the need for routine laboratory monitoring. Management of acute stroke occurring in AF patients who are on anticoagulant therapy poses a significant challenge. In the case of acute ischemic stroke, ongoing anticoagulant therapy is a contraindication to thrombolytic therapy—except when the anticoagulant being used is dabigatran and the hospital has the specific reversal agent idarucizumab available, in which case this reversal agent may be administered, followed by thrombolytic therapy. Initiating or resuming anticoagulation for stroke prevention in patients with acute stroke is likewise a challenge, requiring a decision based on consideration of the extent of cerebral infarction, as well as the extent and cause of any intracerebral hemorrhage. These factors help guide the physician in determining whether to use anticoagulation, which agent to select, and the appropriate timing for initiating or resuming anticoagulant therapy.
