PB1537 - Changes in whole blood platelet aggregation and clotting parameters during pregnancy and postpartum in women with and without heterozygous Factor V Leiden mutation

Tuesday, June 27, 2023

18:30 – 19:30 ET

Room: Exhibition

Presenting Author(s)

Margunn Bye Tøsdal, MD (she/her/hers)

PhD student
Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, Bergen, Norway
Bergen, Hordaland, Norway

Co-Author(s)

TL

Turid Helen Felli Lunde

Researcher/MSc
Department of Immunology and Transfusion Medicine, Haukeland University Hospital, Bergen, Norway
Bergen, Hordaland, Norway
TH

Tor Hervig

MD, Prof.
Department of Clinical Science, University of Bergen, Bergen, Norway
Bergen, Hordaland, Norway
CS

Chen Sun

MD, PhD
Department of Obstetrics and Gynecology, Haukeland University Hospital, Bergen, Norway
Bergen, Hordaland, Norway
SS

Sverre Sandberg

MD, Prof.
Norwegian Organization for Quality Improvement of Laboratory Examinations (Noklus), Haraldsplass Deaconess Hospital, Bergen, Norway
Bergen, Hordaland, Norway
MH

Marit Hellum

Researcher, PhD
Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Oslo, Oslo, Norway
CH

Carola Elisabeth Henriksson, MD

MD, Associate professor
Institute of Clinical Medicine, University of Oslo, Oslo, Norway
Oslo, Oslo, Norway
Ann Helen Kristoffersen, MD, PhD

MD, PhD
Department of Medical Biochemistry and Pharmacology, Haukeland University Hospital, Bergen, Norway
Bergen, Hordaland, Norway

Background: Pregnancy and the postpartum period are hypercoagulable states with increased risk for venous thromboembolism (VTE). However, there are scarce data on platelet activity and clot formation in whole blood in pregnant women both with and without inherited thrombophilia.

Aims: To describe the course of whole blood platelet aggregation and clotting parameters (thromboelastography) throughout pregnancy and postpartum in healthy pregnant women with and without heterozygous Factor V Leiden mutation (FVL).

Methods: Pregnant women with (n=22) and without (n=22) heterozygous FVL were included. Blood samples were collected at four time-points during gestation and three after delivery. Platelet aggregation potential was evaluated with multiple electrode impedance aggregometry (MEA) (Multiplate® (Roche)) by adding the agonists adenosine diphosphate (ADP), arachidonic acid (ASPI) and thrombin receptor-activating peptide-6 (TRAP), and quantified as the area under the aggregation curve (AUC). Clotting in whole blood were evaluated using TEG® 5000 thromboelastograph (TEG) (Haemonetics). Differences between the two groups, and between time-points, were evaluated by mixed-effects models (GraphPad Prism version 9.4). A significance level of p< 0.05 was used, and correction for multiple comparisons was performed by Dunnett's multiple comparisons test. The study was approved by the regional ethics committee (REK-ID 2016/1083) and written informed consent obtained from each participant.

Results: Platelet aggregation decreased during pregnancy (MEA, all agonists), with statistically significant lower AUC in week 28-30 and week 36-38 compared with the other time-points (Figure 1). On the other hand, the TEG parameter maximum amplitude (MA) increased throughout pregnancy, indicating increased platelet activation. Other TEG parameters indicated increasing hypercoagulability during pregnancy (Table 1). There were no statistically significant differences between pregnant women with and without FVL.

Conclusion(s): TEG MA increased during late pregnancy indicating platelet activation. Simultaneously decreased platelet response to agonists might be explained by platelet exhaustion. No differences between pregnant women with and without FVL were found.