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Published on: July 3, 2014
Vitamin K antagonists-associated cerebral hemorrhages: what are their characteristics?
Nelly Dequatre-Ponchelle1, Hilde Hénon, Marta Pasquini
1Department of Neurology, University Lille Nord de France, UDSL, CHU Lille, EA 1046, F-59000 Lille, France.
Insights
Vitamin K antagonists (VKAs) do not cause intracerebral hemorrhages (ICH) but impact their volume differently based on location. VKAs increase nonlobar ICH volume, suggesting varied vasculopathy susceptibility.
Area of Science:
- Neurology
- Vascular Medicine
- Pharmacology
Background:
- Aging populations face increasing rates of intracerebral hemorrhages (ICH) linked to vitamin K antagonists (VKAs).
- The precise role of VKAs as causes versus risk factors for ICH remains debated.
- Understanding VKAs-ICH specificities is crucial for managing anticoagulation in elderly patients.
Purpose of the Study:
- To investigate the specific characteristics of VKAs-associated intracerebral hemorrhages (VKAs-ICH).
- To determine if VKAs act as causes or risk factors for ICH.
- To explore the influence of VKAs on ICH volume based on anatomical location and underlying vasculopathy.
Main Methods:
- Compared baseline characteristics of 545 spontaneous ICH patients, with and without VKA use.
- Analyzed ICH characteristics, including volume, based on anatomical distribution (lobar vs. nonlobar).
- Utilized multiple linear regression to assess the impact of VKAs on ICH volume, considering vasculopathy (cerebral amyloid angiopathy vs. deep perforating arteries).
Main Results:
- VKAs-ICH constituted 15% of the cohort (83 patients).
- VKA use did not alter the anatomical distribution of ICH.
- VKAs significantly increased nonlobar ICH volume (25 mL vs. 12 mL, P=0.002) but not lobar ICH volume (26 mL vs. 30 mL, P=0.507).
Conclusions:
- Similar ICH distribution in VKA users and non-users suggests VKAs are not direct causes of ICH.
- Different impacts of VKAs on ICH volume by location indicate varying susceptibility of underlying vasculopathies.
- Findings may inform tailored therapeutic strategies for VKA-associated ICH based on location and vasculopathy.
Background And Purpose:
The high prevalence of atrial fibrillation in aging populations leads to an increasing incidence of vitamin K antagonists-associated intracerebral hemorrhages (VKAs-ICH). It remains unclear whether VKAs are causes or risk factors for ICH. We aimed at identifying the specificities of VKAs-ICH.
Methods:
We compared baseline characteristics of 545 consecutive patients receiving or not receiving VKAs before admission for spontaneous ICH. To determine whether the influence of VKAs depends on the underlying vasculopathy, that is, cerebral amyloid angiopathy in lobar, and deep perforating arteries vasculopathy in deep ICH, we compared characteristics of ICH (including volume) according to the anatomic distribution of ICH in multiple linear regression.
Results:
VKAs-ICH accounted for 83 patients, that is, 15% (95% confidence intervals, 12-18) of ICH in our cohort. The use of VKAs did not influence anatomic distribution of ICH. The impact of VKAs on ICH volume differed according to ICH location: in nonlobar ICH, VKAs use was associated with significant larger ICH volumes (median volume 25 mL vs 12 mL; P=0.002). In lobar ICH, VKAs use did not influence the volume (median 26 mL vs 30 mL; P=0.507).
Conclusions:
A similar anatomic distribution of ICH in patients with or without VKAs suggests that VKAs should not be considered as a cause of ICH because both locations are usually due to different vasculopathies (deep perforating arteries vasculopathy in deep and cerebral amyloid angiopathy in lobar). The different impact of VKAs on ICH volumes according to location suggests a different susceptibility of these vasculopathies to VKAs. This finding may lead to specific therapeutic strategies.
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