High levels of Lipoprotein (a) (Lp(a)) have been associated with atherosclerotic cardiovascular disease and Deep Venous Thrombosis (DVT). Although, there is many studies demonstrating consistent data between the direct dose-dependent risk of Lp(a) and cardiovascular disease, no solid conclusion has been achieved regarding their contribution to the risk of developing the first and recurrent venous thrombosis. The aim of this study was to evaluate the extent to which high level of Lp(a) is associated with hypercoagulability and/or hypofibrinolysis in patients with spontaneous DVT.

Between January 2017 to January 2020, 152 unprovoked DVT patients were enrolled. With Lp(a) ≥75 nmol/L as cut-off point, patients were divided into high Lp(a) group and low Lp(a) group. Blood biochemistry tests and clinical profile of patients were considered. In order to achieve the goal, Lp (a) and its association with D-dimer, PAI-1, Thrombin/Plasmin generation, and clinical outcomes of unprovoked DVT patients were assessed.

In a total of 152 patients 41 (27%) showed high Lp(a) levels. The results point out a significant difference of D-dimer among groups, with higher prevalence of abnormal D-dimer (> 500 ng/mL) in patients with high Lp(a) (p < 0.05). For thrombin generation, Lag Time (LT) and Maximum Absorbance (MA) parameters showed a significant difference among groups (p < 0.05). Correlation analysis suggested an association between Lp(a) with D-dimer (r = 0.167, p < 0.05), and Lp(a) with LT-Thrombin Generation (r = 0.192, p < 0.05).Multivariate logistic regression showed that higher Lp(a) level was independently associated with D-dimer, LT and MA of Thrombin Generation. No significant difference or association was found regarding PAI-1, Plasmin Generation and Lp (a).

This was the first study to evaluate the association of Lp (a) with D-dimer, PAI-1 and Thrombin/Plasmin generation in unprovoked DVT patients. Theses patients without any hereditary or acquired thrombophilia, showed higher prevalence of abnormal D-dimer levels and faster production of Thrombin after two years of clinical event. No association was found among Lp (a) and PAI-1 or plasmin generation. These results suggest that hypercoagulability may be implicated in the association among Lp (a) and unprovoked DVT patients, but not hypofibrinolysis.