Lipoprotein(a) plasma levels and coagulation biomarkers: Results from a comprehensive laboratory assessment in an angiographically controlled cardiovascular cohort

Background: Lipoprotein(a) [Lp(a)] is a causal risk factor for coronary artery disease (CAD), with proposed prothrombotic properties besides proatherogenic effects. However, the association between Lp(a) and coagulation remains controversial so far. Objective: This study examined this relationship in subjects with or without angiographically documented CAD. Methods: Plasma levels of Lp(a) and coagulation biomarkers were assessed in clinically stable subjects undergoing elective coronary angiography. Subjects taking any anticoagulant therapy were excluded. The coagulation panel included coagulant activities of factors II, V, VII, VIII, IX, X, XI, and XII, von Willebrand factor antigen (vWF:Ag), thrombin generation assay (TGA), total tissue factor pathway inhibitor (TFPI), and activated factor VII-antithrombin (FVIIa-AT) complex. Lp(a) threshold values were defined according to the European Atherosclerosis Society consensus statement: normal <30 mg/dL, intermediate 30 to 50 mg/dL, and high >50 mg/dL. Results: Complete laboratory data were available for 383 subjects (males 75.3%; mean age 68.2 ± 9.7 years): 65 subjects had normal coronary arteries, 51 subjects had coronary stenosis <50%, and 267 subjects had coronary stenosis ≥50%. A modest yet significant increase in FV coagulant activity (FV:C) from low to high Lp(a) plasma levels was found and confirmed after adjustment for potential confounding factors. No differences were observed for all the other coagulant activities, vWF:Ag, total TFPI, FVIIa-AT levels, or TGA parameters. Conclusion: In this pilot study, no major contribution of Lp(a) plasma levels was observed in modulating coagulation phenotype, as evaluated by multiple biomarkers. High Lp(a) plasma levels were associated with only a mild increase in FV:C.