A process that prevents blood clots from growing and becoming problematic.
Tightly regulated and necessary to control thrombus propagation and maintain blood fluidity.
The activation of coagulation by tissue injury and inflammation results in the deposition of fibrin containing thrombus, and to avoid excessive thrombus and to allow thrombus to be remodeled and cleared as tissues heal, cross-linked fibrin is broken down by plasmin.
It has two types: primary fibrinolysis and secondary fibrinolysis.
Fibrinolysis results in the release of fibrin degradation products, the smallest of these is D dimer.
The primary type is a normal body process.
Secondary fibrinolysis is the breakdown of clots due to a medicine, a medical disorder, or some other cause.
A fibrin clot, the product of coagulation, is broken down by fibrinolysis.
The main enzyme of fibrinolysis is plasmin, which cuts the fibrin mesh at various places.
Fibrinolysis leads to the production of circulating fragments that are cleared by other proteases or by the kidney and liver.
Plasmin is produced in an inactive form, plasminogen, in the liver.
Plasminogen itself cannot cleave fibrin, but has an affinity for it, and is incorporated into the clot when it is formed.
Tissue plasminogen activator (t-PA) and urokinase are the agents that convert plasminogen to the active plasmin, initiating fibrinolysis.
t-PA is released into the blood very slowly by the damaged endothelium of the blood vessels.
t-PA breaks the clot down after several days.
Plasminogen becomes entrapped within the clot when it formed, so it only slowly activated to break down the fibrin mesh.
Plasminogen activator inhibitor-1 and plasminogen activator inhibitor-2 (PAI-1 and PAI-2) inhibit t-PA and urokinase.
Plasmin itself further stimulates plasmin generation by producing more active forms of both tissue plasminogen activator (tPA) and urokinase.
Alpha 2-antiplasmin and alpha 2-macroglobulin inactivate plasmin.
Plasmin activity is also reduced by thrombin-activatable fibrinolysis inhibitor (TAFI), which modifies fibrin to make it more resistant to the tPA-mediated plasminogen.
When plasmin breaks down fibrin, a number of soluble fibrin degradation products (FDPs) are formed.
Fibrin degradation products compete with thrombin, slowing clot formation by preventing the conversion of fibrinogen to fibrin.
The thrombin clotting time (TCT) test, which is prolonged in a person that has active fibrinolysis.
Fibrin degradation products, and specifically, the D-dimer, can be measured using antibody-antigen technology
The D-dimer test is more specific than the thrombin clotting time and confirms that fibrinolysis has occurred.
The D-dimer test is used to indicate deep-vein thrombosis, pulmonary embolism, DIC and efficacy of treatment in acute myocardial infarction.
A more rapid detection of fibrinolytic activity , is possible with thromboelastometry in whole blood.
A test of overall fibrinolysis can be measured by a euglobulin lysis time (ELT) assay.
The euglobulin lysis time measures fibrinolysis by clotting the euglobulin fraction (primarily the important fibrinolytic factors fibrinogen, PAI-1, tPA, alpha 2-antiplasmin, and plasminogen) from plasma and then observing the time required for clot dissolution.
A shortened lysis time indicates a hyperfibrinolytic state and bleeding risk, and can be seen in liver disease, PAI-1 deficiency or alpha 2-antiplasmin deficiency, and after administration of DDAVP or after severe stress.
Rare congenital disorders of the fibrinolytic system have been documented.
Excess levels of PAI and alpha 2-antiplasmin have been implicated in the metabolic syndrome and various other disease states.
Acquired disturbance of fibrinolysis occurs with trauma suffering from an overwhelming activation of tissue factor and thus massive hyperfibrinolysis.
The fibrinolytic system is linked to control of inflammation.
Plasmin, lyses fibrin clots, and cleaves the complement system component C3, fibrin degradation products and has vascular permeability inducing effects.
In a process called thrombolysis (the breakdown of a thrombus),
Fibrinolytic drugs are used in thrombolysis to dissolve a thrombus blocking the coronary artery, or after a stroke to allow blood flow back to the affected part of the brain, in the event of a massive pulmonary embolism.
The term thrombolysis refers to the dissolution of the thrombus.
The term fibrinolysis refers specifically to the agents causing fibrin breakdown in the clot.
Aminocaproic acid (ε-aminocaproic acid) and tranexamic acid are antifibrinolytics used as inhibitors of fibrinolysis.
Antifibrinolytics may be beneficial in patients with hyperfibrinolysis because they arrest bleeding.