Key result
Early initiation of antiplatelets or oral anticoagulants after hemorrhagic transformation in acute ischemic stroke was not associated with an increased risk of hemorrhage exacerbation compared to late initiation.
Why the study?
Evidence guiding the timing of antiplatelet and OAC therapy after HI versus PH is limited and inconsistent, causing substantial variation in clinical practice.
Does early initiation of antithrombotic therapy prevent adverse outcomes without increasing hemorrhage exacerbation in acute ischemic stroke patients with hemorrhagic transformation?
Cross-Sectional (n=748)
Yes
Does early initiation of antithrombotic therapy prevent adverse outcomes without increasing hemorrhage exacerbation in acute ischemic stroke patients with hemorrhagic transformation?
Odds Ratio: 0.65 (95% CI 0.15–2.81)
p-value: p=0.561
Early initiation of antithrombotic therapy following hemorrhagic transformation in acute ischemic stroke appears safe and does not significantly increase the risk of hemorrhage exacerbation, while excessive delays in OAC initiation may increase thromboembolic risk.
Early antithrombotic initiation after HT may be safe; leaves open optimal timing pending randomized trials.
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 <0.001). There were no statistically significant differences in HT exacerbation and composite outcomes (30‐day), as well as vascular death and unfavorable functional outcomes (90‐day), between patients who received same‐day, early (HI, <1 day; PH, <3 days), or late (HI, >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 <0.001). Although HT exacerbation rates (30‐day) were comparable between early (HI, <7 days; PH, <15 days) and late (HI, >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.
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Hejazian et al. (2026) conducted a cross-sectional in Acute ischemic stroke with hemorrhagic transformation (n=748). Early initiation of antithrombotic therapy (antiplatelets or OACs) vs. Late initiation of antithrombotic therapy was evaluated on 30-day hemorrhagic transformation (HT) exacerbation (early vs late antiplatelet after hemorrhagic infarction) (OR 0.65, 95% CI 0.15-2.81, p=0.561). Early initiation of antiplatelets or oral anticoagulants after hemorrhagic transformation in acute ischemic stroke was not associated with an increased risk of hemorrhage exacerbation compared to late initiation.
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