Key result
NOAC-related intracerebral hemorrhage was associated with a lower likelihood of severe neurological deficit on admission compared with VKA-related hemorrhage (OR 0.44; 95% CI 0.22-0.85).
Why the study?
Does NOAC use compared to VKA use reduce baseline hematoma volume and neurological severity in patients presenting with anticoagulant-related intracerebral hemorrhage?
Observational (n=196)
Yes
Does NOAC use compared to VKA use reduce baseline hematoma volume and neurological severity in patients presenting with anticoagulant-related intracerebral hemorrhage?
Odds Ratio: 0.44 (95% CI 0.22–0.85)
Absolute Event Rate: 37% vs 55.3%
p-value: p=0.025
In patients with anticoagulant-related intracerebral hemorrhage, prior use of NOACs is associated with significantly smaller baseline hematoma volumes and lower odds of severe neurological deficits compared to VKAs.
May support NOAC preference in anticoagulant-related ICH; leaves open causality and needs RCTs before practice change.
Background and Purpose- The aim of this study was to prospectively validate our prior findings of smaller hematoma volume and lesser neurological deficit in nonvitamin K oral anticoagulant (NOAC) compared with Vitamin K antagonist (VKA)-related intracerebral hemorrhage (ICH). Methods- Prospective 12-month observational study in 15 tertiary stroke centers in the United States, Europe, and Asia. Consecutive patients with premorbid modified Rankin Scale score of <2 with acute nontraumatic anticoagulant-related ICH divided into 2 groups according to the type of anticoagulant: NOAC versus VKA. We recorded baseline ICH volume, significant hematoma expansion (absolute [12.5 mL] or relative [>33%] increase), neurological severity measured by National Institutes of Health Stroke Scale score, 90-day mortality, and functional status (modified Rankin Scale score). Results- Our cohort comprised 196 patients, 62 NOAC related (mean age, 75.0±11.4 years; 54.8% men) and 134 VKA related (mean age, 72.3±10.5; 73.1% men). There were no differences in vascular comorbidities, antiplatelet, and statin use; NOAC-related ICH patients had lower median baseline hematoma volume (13.8 [2.5-37.6] versus 19.5 [6.6-52.0] mL; P=0.026) and were less likely to have severe neurological deficits (National Institutes of Health Stroke Scale score of >10 points) on admission (37% versus 55.3%, P=0.025). VKA-ICH were more likely to have significant hematoma expansion (37.4% versus 17%, P=0.008). NOAC pretreatment was independently associated with smaller baseline hematoma volume (standardized linear regression coefficient:-0.415 [95% CI, -0.780 to -0.051]) resulting in lower likelihood of severe neurological deficit (odds ratio, 0.44; 95% CI, 0.22-0.85) in multivariable-adjusted models. Conclusions- Patients with NOAC-related ICH have smaller baseline hematoma volumes and lower odds of severe neurological deficit compared with VKA-related ICH. These findings are important for practicing clinicians making anticoagulation choices.
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Lioutas et al. (2018) conducted an observational in acute nontraumatic anticoagulant-related intracerebral hemorrhage (n=196). Nonvitamin K oral anticoagulant (NOAC) vs. Vitamin K antagonist (VKA) was evaluated on severe neurological deficit (National Institutes of Health Stroke Scale score of >10 points) on admission (OR 0.44, 95% CI 0.22-0.85, p=0.025). NOAC-related intracerebral hemorrhage was associated with a lower likelihood of severe neurological deficit on admission compared with VKA-related hemorrhage (OR 0.44; 95% CI 0.22-0.85).
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