Lipoprotein(a) (Lp(a)) is a low-density lipoprotein (LDL)–like particle and an established independent risk factor for cardiovascular disease. Its plasma concentration and antifibrinolytic properties are largely genetically determined, primarily by variation in the LPA gene, and in particular, by the number of kringle IV type 2 repeats. Lp(a) contributes to atherogenesis partly through its structural similarity to LDL, promoting cholesterol deposition within the vascular wall. Beyond its proatherogenic effects, Lp(a) plays a key role in acute cardiovascular events through pro-inflammatory and prothrombotic mechanisms. Elevated Lp(a) levels promote a prothrombotic state by increasing tissue factor expression andaccelerating activation of the coagulation cascade. Simultaneously, Lp(a) enhances plaque inflammation and vulnerability by stimulating monocyte activation and through the presence of oxidized phospholipids on its surface. Its structural homology with plasminogen further confers antifibrinolytic properties, allowing Lp(a) to competitively inhibit plasminogen binding to fibrin and impair fibrinolysis. This effect is compounded by increased levels of plasminogen activator inhibitor-1 (PAI-1) and a dysregulation of plasminogen activators (tPA, uPA), plasmin, and other fibrinolytic modulators. The resulting thrombotic risk reflects the dynamic balance between coagulation and fibrinolysis, which can be evaluated using global assays such as overall hemostatic potential. Although novel Lp(a)-lowering therapies achieve substantial reductions in circulating Lp(a) concentrations, their effects on hemostatic balance and clinical outcomes remain to be fully elucidated. This review summarizes current evidence on the role of Lp(a) in coagulation and fibrinolysis, with particular emphasis on the complex interplay between its concentration, structure, genetic deteminants, and contribution to cardiovascular risk.