[The new coagulation cascade and its possible influence on the delicate balance between thrombosis and hemorrhage].

The article published by Navarro et al1 in this issue of Revista Española de Cardiología reports the experience of 4 anticoagulation units located in large referral hospitals in Spain. The article also illustrates the appropriateness of monitoring treatment in specialist units to maintain the level of anticoagulation within the very narrow margin that allows prevention of thrombosis without causing bleeding complications. All thrombotic processes have their origin in the dysfunction or rupture of the vascular endothelium, leading to release of tissue factor, which initiates the process of coagulation, and of collagen and von Willebrand factor, which initiates adhesion and activation of platelets. Alteration of the homeostatic balance between prothrombotic and antithrombotic factors during anticoagulation therapy can result in insufficient inhibition of coagulation (thrombosis) or the occurrence of bleeding due to excessive antithrombotic treatment. The interpretation of the coagulation process described by MacFarlane2 in 1964 (the “MacFarlane cascade”) has been of use for many years in beginning to understand the complex problem of thrombus formation. According to MacFarlane, there are 2 pathways: the extrinsic pathway, involving tissue factor and factor VII, and the intrinsic pathway, in which factors XII, XI, IX, VIII, and V participate. Both pathways converge to activate factor X and lead to transformation of prothrombin into thrombin and, through the action of thrombin, of fibrinogen into fibrin. The role of platelets in coagulation was considered independent. During the following 3 decades, numerous studies were undertaken, culminating in almost simultaneous publications from groups in Houston (Schafer et al3) and The New Coagulation Cascade and Its Possible Influence on the Delicate Balance Between Thrombosis and Hemorrhage Francisco Pérez-Gómeza and Ramón Boverb