Fibrinolysis is the dissolving of a thrombus by the action of enzymes. Enzymes are proteins produced in the body that bring about a chemical reaction. Plasmin is an enzyme that is very active in breaking down fibrin. Plasmin helps to dissolve a thrombus and limits clot formation by digesting coagulation factors V, VIII, XII, and prekallikrein. The inhibition and activation of plasminogen (the inactive precursor of plasmin) modulate fibrinolysis.

A hypercoagulable state is a condition in which the blood is more readily coagulated or clotted than is normal. The formation of a hemostatic clot requires the coordinated action of a number of factors. A balance exists between the formation and dissolution of a thrombus (clot) in the normal physiologic response. At times, congenital (hereditary) defects or acquired defects destroy this balance, which can result in abnormal bleeding or in abnormal thrombosis. In 80–90% of people with a thrombosis, a cause can be defined. In 50–80% of these, a hereditary or acquired defect is the cause. Most hypercoagulable states are associated with a spontaneous onset of deep venous thrombosis at an early age.

Abnormal thrombosis may result from deficiencies in protein C and protein S, activated protein C resistance, abnormalities in the antithrombin system, tissue plasminogen activator or factor XII deficiencies, prothrombin mutations, platelet aggregation (clumping) induced by heparin (an anticoagulant agent), antiphospholipid antibody syndrome, lupus anticoagulant, or hyperhomocysteinemia.