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External Validation of Six Scores Differentiating Atherosclerotic vs. Embolic Large Vessel Occlusion

Sakuta, K.; Nakada, R.; Sakai, K.; Okumura, M.; Kida, H.; Motegi, H.; Nagayama, G.; Tachi, R.; Miyagawa, S.; Komatsu, T.; Mitsumura, H.; Yaguchi, H.; Iguchi, Y.

2026-02-14 neurology
10.64898/2026.02.11.26346119 medRxiv
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PurposeIntracranial atherosclerotic disease-related large vessel occlusion (ICAD-LVO) presents distinct challenges, particularly regarding the high risk of reocclusion and the need for specific management strategies. While several prediction scores exist to differentiate ICAD-LVO from embolic LVO (EMB-LVO), their external validity remains unproven. We aimed to externally validate six established prediction scores for differentiating the two. MethodsWe analyzed data from a prospectively maintained, two-center stroke registry (June 2021-March 2025). Consecutive patients who underwent mechanical thrombectomy and had complete clinical and imaging data necessary for calculating six scores (ISAT, REMIT, ABC2D, ATHE, ICAS-LVO, and Score-ICAD) were included. LVO etiology was defined based on angiographic findings during endovascular treatment. The discriminative performance of each score was assessed using the area under the receiver operating characteristic curve (AUC). ResultsOf 1,288 screened admissions, 91 patients met the inclusion criteria (ICAD-LVO, n = 18; embolic occlusion, n = 73). The AUCs (95% confidence interval) for differentiating etiology were: ISAT, 0.870 (0.664-1.000; P = 0.064); REMIT, 0.793 (0.676-0.911; P <0.001); Score-ICAD, 0.707 (0.582-0.833; P = 0.013); ABC2D, 0.627 (0.504-0.751; P = 0.095); ATHE, 0.600 (0.451-0.749; P = 0.230); and ICAS-LVO, 0.465 (0.301-0.630; P = 0.650). ConclusionIn this external validation, REMIT demonstrated the most robust and statistically significant discrimination between ICAD-LVO and EMB-LVO. Overall, scores incorporating imaging features outperformed those relying on clinical variables. These findings support the concept that ICAD-LVO represents a distinct pathophysiological entity from embolic occlusion and that accurate mechanism inference requires comprehensive imaging assessment of intracranial atherosclerotic disease beyond the occlusion site.

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