Symptomatic hematoma expansion in DOAC-associated intracerebral hemorrhage increased to 25.0% at DOAC levels ≥300 ng/mL, indicating a potential threshold effect.
Do higher DOAC plasma levels increase the risk of hematoma expansion in patients with DOAC-associated intracerebral hemorrhage?
Higher DOAC plasma levels show a nonsignificant trend toward increased risk of symptomatic hematoma expansion in DOAC-associated intracerebral hemorrhage.
Tasa de eventos absoluta: 0% vs 0%
Introduction: DOACs are associated with an increased risk of hematoma expansion (HE) in spontaneous ICH, yet the critical DOAC plasma levels influencing this risk are unknown. Methods: A retrospective multicenter study on DOAC-associated ICH across 10 centers in Germany and Taiwan. Patients with emergent DOAC plasma levels upon admission were included. DOAC levels were categorized using proposed cut-offs and ROC analysis. HE was defined as a ≥35% increase in hematoma volume between admission and 48-hour CT scans, with symptomatic HE defined as a concurrent ≥4-point NIHSS increase. Multivariable regression analysis explored associations between DOAC cut-offs and HE, adjusting for baseline ICH volume, onset-to-imaging time, systolic blood pressure and reversal use. Results: In this preliminary analysis, 197 patients were included (57% male; median age 81 75–84 years; median NIHSS 12 IQR 7–19). Most received FXa inhibitors (98%), four dabigatran (median DOAC level: 101.5 ng/mL IQR 51–187.5). Overall, HE within 48 hours occurred in 58 of 197 patients (29.4%) and symptomatic HE in 23 patients (11.7%). The frequency of symptomatic HE increased stepwise with higher DOAC levels: 9.2% below 100 ng/mL, 14.1% at ≥100 ng/mL, 16.4% at ≥150 ng/mL, 20.5% at ≥200 ng/mL, 23.8% at ≥250 ng/mL and 25.0% at ≥300 ng/mL. While unadjusted analysis indicated higher rates of symptomatic HE at ≥200 ng/mL (p=0.04), multivariable models did not reach statistical significance (aOR 2.0, 95%CI 0.7–5.8; p=0.21 at ≥200 ng/mL). A nonsignificant trend toward higher risk was observed at very high levels (aOR 3.0, 95%CI 0.8–10.7; p=0.09 at ≥300 ng/mL). Conclusions: The risk of symptomatic HE may increase with higher DOAC plasma levels in patients with DOAC-associated ICH, with a possible threshold effect at very high levels. These preliminary findings require further analysis of the full multicenter cohort to assess the predictive value of specific DOAC thresholds for clinical risk stratification.
Schoene et al. (Thu,) reported a other. Symptomatic hematoma expansion in DOAC-associated intracerebral hemorrhage increased to 25.0% at DOAC levels ≥300 ng/mL, indicating a potential threshold effect.