Fibrinolysis occurs after coagulation, and is the process where a fibrin clot is broken down.
Plasmin is produced in an inactive form, plasminogen, in the liver. Although plasminogen cannot cleave fibrin, it still has an affinity for it, and is incorporated into the clot when it is formed.
Tissue plasminogen activator (tPA) is what converts plasminogen to plasmin. Thus allowing fibrinolysis to occur. This is released into the blood by the cells of the healthy endothelium neighbouring the clot.
tPA cleaves plasminogen, which starts fibrinolysis, though tPA is inhibited by other chemicals in the bloodstream. Alpha-2-antiplasmin, and plasminogen activator inhibitor (PAI) serve to turn off tPA.
When plasmin breaks down fibrin, a number of soluble parts are produced. These are called fibrin degradation products (FDPs). FDPs compete with thrombin, and so slow down the conversion of fibrinogen to fibrin (slows down clot formation). This effect can be seen in the TCT or thrombin clotting time test, which is longer in a person who has recently undergone fibrinolysis.
FDPs, and a specific FDP, the D-dimer, can be measured using antibody-antigen technology. This is more specific than the TCT, and virtually confirms that fibrinolysis has occurred.
It is important to know if fibrinolysis has recently happened, as this can indicate deep vein thrombosis or a pulmonary embolism.
The two main drugs that are used are:
Physiological fibrinolysis
The main enzyme of fibrinolysis is plasmin. Plasmin cleaves fibrin in multiple locations and acts to dissolve a fibrin clot.Treatment using fibrinolysis
Fibrinolytic drugs are given after a heart attack to dissolve the thrombus blocking the coronary artery.