LAUSR

BACKGROUND Cardiogenic cerebral embolism is one of the most common causes of ischemic stroke. In general, cardioembolic stroke is associated with more severe neurological deficits and higher early mortality, as well as a worse functional outcome. Oral anticoagulant (OAC) therapy could reduce the risk of stroke significantly. However, several limitations have led to it being underused, which raises the failure of anticoagulant therapy. This study aimed to investigate the patients with atrial fibrillation presented cardioembolic stroke who underwent OAC therapy, and to assess treatment efficacy, and outcomes, especially the international normalized ratio (INR) value in the acute phase. METHODS Clinical data of 306 patients with cardioembolic stroke and etiology of atrial fibrillation were retrospectively analyzed, and demographics, cardiovascular risk factors, embolic cardiopathy, CHADS2 and CHA2DS2-VASc score, HAS-BLED score, INR value, TOAST subtypes, OCSP classification, modified Rankin Scale (mRS) scores and prognosis were evaluated. RESULTS The median score on the CHADS2 and CHA2DS2-VASc scales was 3 and 4, respectively; The median score on the HAS-BLED scale was 2. Only 33 patients (10.8%) were in therapeutic INR range at the onset of stroke. In the acute phase, 233 patients (76.1%) continued to use OAC therapy, and 73 patients were suspended. Eighteen patients (24.7%) resumed treatment after an average of 32 days. Thirty-nine of 251 survivors with nonvalvular atrial fibrillation were modified to novel oral anticoagulants (NOACs). At 3 months follow-up, patients with INR ≥1.7 had significantly better prognosis than those with INR <1.7, both in the percentage of patients with functional independence (78.9% vs. 41.2%) and in mortality (7.0% vs. 25.0%) (P<0.001). CONCLUSIONS Patients presented cardioembolic stroke despite being treated with OAC, especially those with a subtherapeutic INR value, raises the failure of anticoagulant therapy. Despite the ineffectiveness of the OAC, the prognosis is better when the INR ≥1.7 at the initiation of the stroke.