Under normal conditions, hemostasis is the process which results in clot formation upon vascular injury and thereby prevents further blood loss. Platelets become activated and form a platelet plug or aggregate and activation of the coagulation system results in the formation of a fibrin network, which stabilizes the platelet plug. In case of deficiency or dysfunction of the hemostatic components, clot formation is impaired leading to a higher risk of bleeding events.
The severity of bleeding, occurring either spontaneously or after specific challenges, depends on the type of the defect present. Congenital bleeding disorders are usually the consequence of inherited genetic mutations (e.g. hemophilia), while acquired bleeding disorders have multiple causes. For example, the treatment of patients with dual antiplatelet therapy for the prevention of new atherothrombotic events comes with an increased risk of bleeding.1 In addition to bleeding assessment tools, several hemostatic tests are employed for the diagnosis of bleeding disorders and the prediction of bleeding events. Limitations of the current hemostatic tests and unknown underlying mechanisms of bleeding underscore the importance of optimizing the identification of patients at risk.