PB0025 - Primary hemostasis, coagulation and fibrinolysis markers in patients with intracranial large vessel occlusion stroke, on admission to hospital

Sunday, July 10, 2022

6:30 PM – 7:30 PM

Location: Exhibition

Presentation Format: In-Person

Presenting Author(s)

AB

Aarazo Barakzie, MSc

MSc. Ph.D. student
Department of Hematology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands
Rotterdam, Zuid-Holland, Netherlands

Co-Author(s)

AB

Agnetha Bruggeman

PhD candidate
Department of Radiology and Nuclear Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands
Amsterdam, Noord-Holland, Netherlands
GD

Gabriëlla Dirks

Research analyst
Department of Hematology, Erasmus University Medical Center, Rotterdam, The Netherlands
Rotterdam, Zuid-Holland, Netherlands
DW

Diederik W.J. Dippel

Prof. Dr. neurologist
Department of Neurology, Erasmus MC, University Medical Center, Rotterdam, The Netherlands.
Rotterdam, Zuid-Holland, Netherlands
CB

Charles B. L. M. Majoie

Professor of Neuroradiology
Department of Radiology and Nuclear Medicine, Amsterdam UMC, University of Amsterdam, Amsterdam Neuroscience, Amsterdam, The Netherlands
Amsterdam, Noord-Holland, Netherlands
Moniek P.M. de Maat, PhD

Professor
Department of Hematology, Erasmus University Medical Center Rotterdam, Rotterdam, The Netherlands
Rotterdam, Zuid-Holland, Netherlands

Background: Acute Ischemic Stroke (AIS) is most often caused by thromboembolic occlusion of the cerebral blood vessels. Changes in the primary hemostasis, coagulation, and fibrinolysis systems are important causal factors in thrombus formation but information on the levels at the acute moment of stroke are limited. Better understanding of hemostatic and fibrinolytic factors will help us to predict the risk of developing AIS and effects of treatments.

Aims: To study the levels and activities of primary hemostasis, coagulation, and fibrinolysis markers in patients with AIS.

Methods: We used data from patients with AIS of included in MR CLEAN-NOIV trial. We measured hemostatic factors von Willebrand Factor Antigen (VWF:Ag), ADAMTS13, FVIII, fibrinogen, D-dimer, and tissue-Plasminogen Activator (tPA) in citrated plasma of AIS patients collected on admission to hospital. Hemostatic factors levels and activity were presented as either mean and standard deviation (SD) or median and inter-quartile range (IQR) in case of skewedness.

Results: We included 131 AIS patients. ADAMTS13 activity (mean 65 ± SD 23%, (Ref. 41-129%)) was normal in AIS patients, whereas the levels of VWF:Ag (mean 2.26 ± SD 1.10 U/mL, (Ref. 0.60-1.40 U/mL)), FBG (mean 2.58 ± SD 1.44 g/l (Ref. 1.5-3.6 g/l)), D-dimer (median 1.07 mg/L [IQR 1.47], (Ref. < 0.50 mg/L)), FVIII (median 1.47 U/mL [IQR 1.41], (Ref. 0.60-1.40 U/mL)), and tPA:Ag (median 10.69 ng/ml [IQR 10.97], (Ref. < 10 ng/mL)) were extremely increased in these patients compared to references (Ref). tPA:Ag in 49 patients was extremely high (>511 ng/ml).

Conclusion(s): In patients with AIS, we found increased levels of VWF:Ag, FBG, FVIII, D-dimer and tPA:Ag on admission to hospital. These findings indicate that the primary hemostasis, coagulation, and fibrinolysis systems are disturbed in AIS patients. Increased levels of hemostatic and fibrinolytic markers might be involved in pathogenesis of AIS and clinical failure of AIS thrombolysis treatment.