PB1407 - The increased risk of venous thromboembolism (VTE) in obese pregnant women is due to more prolonged exposure to a procoagulant state.

Background: VTE remains the leading direct cause of maternal death, with obese women over-represented within the data. A better understanding of the pathophysiology underlying the increased risk of VTE in obese pregnant women is needed to develop more effective preventative strategies.

Aims: To characterise the prothrombotic phenotype of obese pregnant women.

Methods: 262 women, grouped by BMI class, were recruited to a British Heart Foundation funded prospective longitudinal study, approved by the West of Scotland Research Ethics Committee. Following written informed consent, blood samples were obtained at the antenatal booking appointment and repeated at 28 weeks’ gestation. Thrombin generation was performed using the Calibrated Automated Thrombogram method. Protein S (PS), and fibrinogen were assayed by the ACL TOP analyser. Tissue factor pathway inhibitor (TFPI), and plasminogen activator inhibitor-1(PAI-1) were quantified by ELISA.

Results: At booking, endogenous thrombin potential (ETP) was significantly higher in obese (p=0.0003) compared to lean women (Fig.1). By 28 weeks, ETP had increased and there was no longer any difference between BMI groups. The increase in ETP with advancing pregnancy was significantly greater in lean (19.92%) compared to obese class-II women (-3.37%), (p=0.025). A similar pattern was observed for peak thrombin, velocity index and PAI-1. Fibrinogen was significantly higher in obese compared to lean women at booking (p < 0.001) and remained higher, whilst increasing, with advancing gestation (p < 0.001) (Fig.2).
TFPI and PS were significantly higher at booking in obese compared to lean women (p < 0.001 and p=0.03, respectively), with a greater percentage decrease by 28 weeks (TFPI: lean -6.9%, obese class-III -24%; PS: lean -3.8%, obese class-III -15.2%).

Conclusion(s): Obese women are exposed to the prothrombotic state earlier in pregnancy than lean women which, accompanied by the greater percentage reduction in TFPI and PS by 28 weeks’ gestation, may explain why this group is at increased risk of death from VTE.