Incorporation of fragment X into fibrin clots renders them more susceptible to lysis by plasmin

Bleeding, the serious complication of thrombolytic therapy with tissue type plasminogen activator (t-PA), is a result from lysis of fibrin in hemostatic plugs and from the systemic lytic state caused by unopposed plasmin. It suggests that structural changes resulting from incorporation of fragment X into clots promote their lysis and the attenuation of thrombolytic therapy-induced fragment X formation might reduce the risk of bleeding.