Fibrinolysis

Fibrinolysis occurs after coagulation, and is the process where a fibrin clot is broken down.

Physiological fibrinolysis

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.

Treatment using fibrinolysis

The two main drugs that are used are:

• Streptokinase - produced by alpha-haemolytic Streptococcus species. This is very effective and cheap, though since it is a bacterial product, the body will build up an immunity to it. For this reason, it is usually given only for a person's first heart attack.
• Recombinant tPA - also very effective, but very expensive. It does not have the immune problems that streptokinase is associated with.

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