{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,19]],"date-time":"2026-08-19T14:05:35Z","timestamp":1787148335997,"version":"build-2736575974"},"reference-count":92,"publisher":"Korean Stroke Society","issue":"2","license":[{"start":{"date-parts":[[2025,5,31]],"date-time":"2025-05-31T00:00:00Z","timestamp":1748649600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"content-domain":{"domain":["j-stroke.org"],"crossmark-restriction":true},"short-container-title":["J Stroke"],"published-print":{"date-parts":[[2025,5,31]]},"abstract":"<jats:p>Anticoagulation is crucial to reducing the risk of cardioembolic strokes, particularly in vulnerable populations such as patients with atrial fibrillation, artificial heart valves, or left ventricular thrombus. Though successful, anticoagulation failure (the occurrence of an ischemic stroke or systemic embolism while receiving therapy) remains a major stroke-care issue. The reason for anticoagulation failure can be below the required threshold, inability to follow up, drug-drug interactions, preexisting hypercoagulable states, or anticoagulant resistance. This failure undermines stroke prevention and requires tailored management, often requiring more drastic or alternative interventions. This review examines what drives anticoagulation failure and explores predictors of this failure in clinical, imaging, and laboratory data. 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