PB1020 - Simultaneous generation of thrombin and plasmin in patients with deep vein thrombosis and high levels of Lipoprotein (a)

Background: The potential pathomechanisms of Lp(a) in Deep Vein Thrombosis (DVT) include its association with oxidized phospholipids that induce PAI-1 production in endothelial cells or the similarity of Lp(a) with plasminogen, which result in decreased plasmin synthesis and fibrinolysis inhibition. Hypercoagulability and/or hypofibrinolysis are associated to the development of thrombosis.

Aims: The aim of this study was to evaluate for the first time the simultaneous thrombin and plasmin generation test (SPT) in patients with Unprovoked DVT who have high plasma levels of LP(a).

Methods: Were included in these study samples of 152 patients from Blood Center at Unicamp SP-Brazil. The demographic characteristics of patients are in table 1. Patients were divided into, TEV-LP(a)+ group: with LP (a) values >75 nmol/L and TEV-LP(a)- group: < 75 nmol/L.

Results: The TEV-LP(a)+ patients, showed higher thrombin generation, demonstrated by a higher maximum of absorbance-MA (p = 0.036). In addition, these patients took longer to initiate the fibrin clot with greater lag time of thrombin-LT (p = 0.028), and were faster in fibrin formation VM (p = 0.017). Plasmin generation remained unchanged, which leads us to think about imbalance between thrombin and plasmin generation, table 2. To assess the sensitivity regarding LP(a) and the change in thrombin parameters, the patients were separated into the 75/90th percentile, and the differences remained significant, except for VM. The second stage of the study was to assess the association of Lp(a) with MA and LT parameters, and although a significant correlation was found between Lp(a) and LT, this was not confirmed in univariate linear regression analysis.

Conclusion(s): Patients with VTE and high levels of LP(a) have higher thrombin generation, which contributes to the hypothesis that high levels of Lp(a) may induce a thrombogenic state. The association of LP(a) with VTE could be explained by a persistent state of hypercoagulability rather than possible hypofibrinolysis.