Fibrinolysis is the dissolution of the clot formation process involving the plasma protein plasminogen. This system of enzymes dissolves blood clots by the lysis of fibrin. Fibrinolysis plays a role as well in other biological processes such as tissue repair, macrophage activation and function, ovulation, and embryo implantation. Fibrinolysis is mediated by plasmin and during blood coagulation, lysis of fibrin by plasmin results in derivation fragments of fibrin called fibrin degradation products (FDP).
Thrombocytopenia is a condition where the circulating platelet count falls below 50,000 platelets per microliter. As a result of such low circulating platelet levels, people have bleeding tendencies similar to those experienced by hemophiliacs (deficiency of Factor VIII), except that bleeding occurs primarily from small capillaries and venules, as opposed to the larger vessels involved with hemophilia. This condition is usually antibody mediated (idiopathic thrombocytopenia), and the cardiac patient can be impacted by either long term heparin therapy (heparin induced thrombocytopenia), or significant platelet loss and sequestration secondary to the extracorporeal circuit.
Heparin induced thrombocytopenia (HIT) complicates heparin therapy in about 2% to 5% of patients undergoing cardiopulmonary bypass. While manifesting mildly without causing excessive bleeding in most patients, it has occasionally led to life threatening hemorrhage, acute arterial thrombosis, myocardial infarction, stroke and limb ischemia. Recent studies found that this condition results from a specific IgG antiheparin antibody which binds to repeating antigenic determinants in heparin. This antiheparin antibody in turn binds to the surface of the platelet. There is no reliable method for predicting which patients will develop HIT.