Early initiation of OACs after parenchymal hematoma was associated with lower 30-day composite outcomes compared to late initiation (3% vs 20.7%; P=0.044), with no difference in HT exacerbation.
Cross-Sectional (n=748)
Yes
Does early initiation of antiplatelets or oral anticoagulants prevent recurrent stroke/systemic emboli without increasing hemorrhagic transformation exacerbation in patients with ischemic stroke and hemorrhagic transformation?
Early initiation of oral anticoagulants after parenchymal hematoma in ischemic stroke patients may reduce systemic thromboembolic events without significantly increasing the risk of hemorrhagic transformation exacerbation.
Absolute Event Rate: 3% vs 20.7%
p-value: p=0.044
Background Evidence to guide the optimal timing of antiplatelet and oral anticoagulants (OACs) therapy after hemorrhagic infarction (HI) versus parenchymal hematoma (PH) is limited and inconsistent, leading to substantial variation in practice. This study's goal was to study the practice pattern and compare clinical outcomes associated with early‐versus‐delayed initiation of antiplatelet/OACs after hemorrhagic transformation (HT). Methods This multicenter, retrospective, cross‐sectional study included patients with acute ischemic stroke and HT. Patients with an HI or PH were categorized by HT to antithrombotic initiation time, and their outcomes—30‐day HT exacerbation, composite outcomes of recurrent stroke/systemic emboli, 90‐day vascular death, and functional outcomes—were compared. Results Of 748 patients, 496 received antiplatelets, and 252 received OACs after HT. The median HT‐to‐antiplatelet time was significantly shorter after HI than PH (1 interquartile range, 0–2 versus 3 interquartile range, 1–5 days; P 1 day; PH, >3 days) antiplatelets after either HI or PH. Among patients on OACs, those with HI had shorter median HT‐to‐OAC time than PH (7 interquartile range, 2–15 versus 15 interquartile range, 7–32 days; P 7 days; PH, >15 days) OAC initiation after either HI or PH, late initiation after PH was accompanied by higher rates of composite outcomes (30‐day) than early initiation (20.7% versus 3%; P =0.044). Regression models adjusted for demographics, National Institutes of Health Stroke Scale, and stroke severity showed no statistically significant association between early initiation of antiplatelets or OACs with HT exacerbation risk. Conclusions Our study found no statistically significant difference in HT exacerbation between early and late initiation of antiplatelets or OACs among patients with HI/PH, while prolonged delay among patients with PH were accompanied by increased systemic thromboembolic events. Although these findings offer preliminary clinical insight, prospective studies are needed.
Hejazian et al. (2026) conducted a cross-sectional in acute ischemic stroke and hemorrhagic transformation (n=748). Early initiation of antiplatelets or OACs vs. Delayed/late initiation of antiplatelets or OACs was evaluated on 30-day composite outcomes of recurrent stroke/systemic emboli (OACs after parenchymal hematoma) (p=0.044). Early initiation of OACs after parenchymal hematoma was associated with lower 30-day composite outcomes compared to late initiation (3% vs 20.7%; P=0.044), with no difference in HT exacerbation.