Journal of Neurology

, Volume 254, Issue 12, pp 1660–1665

Haemostatic genetic variants, ABO blood group and bleeding risk during oral anticoagulant treatment after cerebral ischaemia of arterial origin

  • D. M. O. Pruissen
  • F. R. Rosendaal
  • J. W. Gorter
  • A. A. Garcia
  • L. J. Kappelle
  • A. Algra
  • for the SPIRIT Study Group*
ORIGINAL COMMUNICATION

DOI: 10.1007/s00415-007-0609-5

Cite this article as:
Pruissen, D.M.O., Rosendaal, F.R., Gorter, J.W. et al. J Neurol (2007) 254: 1660. doi:10.1007/s00415-007-0609-5
  • 91 Downloads

Abstract

Oral anticoagulant treatment for secondary prevention after cerebral ischaemia of presumed arterial origin is associated with a higher bleeding rate than cardioembolic stroke. This discrepancy is only partly explained by known bleeding risk factors. Haemostatic genetic variants and AB0 blood group may be involved.

We performed a nested casecontrol study in patients with cerebral ischaemia of presumed arterial origin on anticoagulant treatment (International Normalized Ratio between 3.0–4.5). All 34 cases with non-fatal haemorrhage (10 intracranial and 24 extracranial) and 68 control patients on anticoagulant treatment without such a bleeding were selected from the SPIRIT study. AB0 blood group and 11 haemostatic genetic variants were investigated.

The Thr312Ala variant of the alpha fibrinogen gene was associated with a decreased bleeding risk (odds ratio (OR) 0.3 for Ala/Ala and Thr/Ala versus Thr/Thr genotype; 95% CI 0.1–0.8). Factor V Leiden was associated with an increased bleeding risk (OR 11.6; 95% CI 1.3–103). The APOE2 allele (OR 0.5; 95% CI 0.2–1.7) and the Tyr204Phe variant in the factor XIII subunit A (OR 2.1; 0.9–5) had nonsignificant relationships with bleeding risk. AB0 blood group and 7 other genetic variants in coagulation factors II and XIII, vitamin K epoxide reductase complex, beta fibrinogen and apolipoprotein E were not related with the risk of haemorrhage.

The Ala312Thr variant in the alpha fibrinogen gene is associated with a decreased and factor V Leiden with an increased bleeding risk in patients on anticoagulant treatment after cerebral ischaemia of presumed arterial origin.

Key words

polymorphism ischaemic stroke haemostasis anticoagulant bleeding risk 

Copyright information

© Steinkopff Verlag 2007

Authors and Affiliations

  • D. M. O. Pruissen
    • 1
  • F. R. Rosendaal
    • 2
  • J. W. Gorter
    • 1
  • A. A. Garcia
    • 3
  • L. J. Kappelle
    • 1
  • A. Algra
    • 1
    • 4
  • for the SPIRIT Study Group*
  1. 1.Dept. of Neurology, Rudolf Magnus Institute of NeuroscienceUniversity Medical Center UtrechtThe Netherlands
  2. 2.Dept. of Clinical Epidemiology and HaematologyLeiden University Medical CenterThe Netherlands
  3. 3.Center for Experimental and Molecular MedicineAcademic Medical CenterAmsterdamThe Netherlands
  4. 4.Julius Center for Health Sciences and Primary CareUniversity Medical Center Utrecht, Room STR 6.313UtrechtThe Netherlands

Personalised recommendations