Atrial fibrillation (AF) represents the most common sustained cardiac arrhythmia and substantially inflates the risk of ischemic stroke. In particular, patients with AF present 3- to 5 -fold higher odds of suffering a cerebrovascular event, and approximately one third of all ischemic strokes are caused by AF.1,2 Notably, the primary pathophysiological mechanism underlying stroke in the setting of non-valvular AF is considered to be cardiogenic thromboembolism. Although this is true for the majority of AF patients, a considerable proportion among them is diagnosed with ischemic stroke on the grounds of alternative pathologies.3 Indeed, accumulating evidence suggests that ischemic stroke in patients with AF - especially in those with high CHA2DS2-VASc score e may be attributed in certain cases to athero-thrombotic mechanisms and not to cardio-embolic sequelae.4 To this end, contemporary therapeutic strategies in AF patients after an index cerebrovascular episode often fail to take into consideration alternative causes for stroke occurrence, leading to sub-optimal secondary prevention and missed opportunities for appropriate treatment intensification in this high-risk population. Importantly, initiation and maintenance of oral anticoagulants in AF patients, solely on the basis of risk for cardiogenic embolism, independently of stroke etiology and subtyping, may further blunt accurate risk stratification and effective individualized management in stroke survivors.
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