Activated clotting time

Activated clotting time (ACT), also known as activated coagulation time is a test of coagulation.

The ACT test can be used to monitor anticoagulation effects, such as high-dose heparin before, during, and shortly after procedures that require intense anticoagulant administration, such as cardiac bypass, cardiac angioplasty, thrombolysis, extra-corporeal membrane oxygenation (ECMO) and continuous dialysis. It measures the seconds needed for whole blood to clot upon exposure to an activator of an intrinsic pathway by the addition of factor XII activators.

The clotting time is based on a relative scale and requires a baseline value for a point of comparison due to inconsistencies between the source and formulation of the activator being used. It is usually ordered in situations where the partial thromboplastin time (PTT) test may take an excessive amount of time to process or is not clinically useful. Prolongation of the ACT may indicate a deficiency in coagulation factors, thrombocytopenia or platelet dysfunction. Clotting time measurements can be affected by other drugs that such as Warfarin, aprotinin and GPIIb/IIIa inhibitors.

Activated partial thromboplastin time

The partial thromboplastin time (PTT) or activated partial thromboplastin time (aPTT or APTT) is a medical test that characterizes blood coagulation. Apart from detecting abnormalities in blood clotting, it is also used to monitor the treatment effects with heparin, a major anticoagulant. PTT is a performance indicator of the efficacy of both the “intrinsic” (now referred to as the contact activation pathway) and the common coagulation pathways. It is used in conjunction with the prothrombin time (PT) which measures the extrinsic pathway. Kaolin cephalin clotting time (KccT) is a historic name for the activated partial thromboplastin time.

Activated protein C resistance

Activated protein C resistance (APCR) is a hemostatic disorder characterized by a poor anticoagulant response to activated protein C (APC). This results in an increased risk of venous thrombosis, which can cause problems with circulation, such as pulmonary embolism.

The disorder can be acquired or inherited, the hereditary form having an autosomal dominant inheritance pattern.

Activated protein C (with protein S as a cofactor) degrades Factor Va and Factor VIIIa. Activated protein C resistance is the inability of protein C to cleave Factor Va and/or Factor VIIIa, which allows for longer duration of thrombin generation and may lead to a hypercoagulable state. This may be hereditary or acquired. The best known and most common hereditary form is Factor V Leiden. Acquired forms occur in the presence of elevated Factor VIII concentrations.

Alpha 2-antiplasmin

Alpha 2-antiplasmin (or α2-antiplasmin or plasmin inhibitor) is a serine protease inhibitor (serpin) responsible for inactivating plasmin, an important enzyme that participates in fibrinolysis and degradation of various other proteins. This protein is encoded by the SERPINF2 gene.

American Society of Hematology

The American Society of Hematology (ASH) is the world’s largest professional society serving both clinicians and scientists around the world who are working to conquer blood diseases.

The Society’s mission is to further the understanding, diagnosis, treatment, and prevention of disorders affecting the blood, bone marrow, and the immunologic, hemostatic and vascular systems, by promoting research, clinical care, education, training, and advocacy in hematology.


Anticoagulants (antithrombics, fibrinolytic, and thrombolytics) are a class of drugs that work to prevent the coagulation(clotting) of blood. Such substances occur naturally in leeches and blood-sucking insects. A group of pharmaceuticals called anticoagulants can be used in vivo as a medication for thrombotic disorders. Some anticoagulants are used in medical equipment, such as test tubes, blood transfusion bags, and renal dialysis equipment.

Antiphospholipid syndrome

Antiphospholipid syndrome or antiphospholipid antibody syndrome (APS or APLS), or often also Hughes syndrome, is an autoimmune, hypercoagulable state caused by antiphospholipid antibodies. APS provokes blood clots (thrombosis) in both arteries and veins as well as pregnancy-related complications such as miscarriage, stillbirth, preterm delivery, and severe preeclampsia.

The diagnostic criteria require one clinical event, i.e. thrombosis or pregnancy complication, and two positive blood testsspaced at least three months apart. These antibodies are: lupus anticoagulant, anti-cardiolipin and anti-β2-glycoprotein-I.

Antiphospholipid syndrome can be primary or secondary. Primary antiphospholipid syndrome occurs in the absence of any other related disease. Secondary antiphospholipid syndrome occurs with other autoimmune diseases, such assystemic lupus erythematosus (SLE). In rare cases, APS leads to rapid organ failure due to generalised thrombosis; this is termed “catastrophic antiphospholipid syndrome” (CAPS) and is associated with a high risk of death.

Antiphospholipid syndrome often requires treatment with anticoagulant medication such as heparin to reduce the risk of further episodes of thrombosis and improve the prognosis of pregnancy. Warfarin/Coumadin is not used during pregnancy because it can cross the placenta, unlike heparin, and is teratogenic.


An antiplatelet drug (antiaggregant) is a member of a class of pharmaceuticals that decrease platelet aggregation and inhibit thrombus formation. They are effective in the arterial circulation, where anticoagulants have little effect.

They are widely used in primary and secondary prevention of thrombotic cerebrovascular or cardiovascular disease.


Antithrombin (AT) is a small protein molecule that inactivates several enzymes of the coagulation system. Antithrombin is a glycoprotein produced by the liver and consists of 432 amino acids. It contains three disulfide bonds and a total of four possible glycosylation sites. α-Antithrombin is the dominant form of antithrombin found in blood plasma and has an oligosaccharide occupying each of its four glycosylation sites. A single glycosylation site remains consistently un-occupied in the minor form of antithrombin, β-antithrombin. Its activity is increased manyfold by the anticoagulant drug heparin, which enhances the binding of antithrombin to factor IIand factor X.

Antithrombin III deficiency

Antithrombin III deficiency (abbreviated ATIII deficiency) is a deficiency of antithrombin III. It is a rare hereditary disorder that generally comes to light when a patient suffers recurrent venous thrombosis and pulmonary embolism, and repetitive intrauterine fetal death (IUFD). Inheritance is usually autosomal dominant, though a few recessive cases have been noted.

The patients are treated with anticoagulants or, more rarely, with antithrombin concentrate.

In kidney failure, especially nephrotic syndrome, antithrombin is lost in the urine, leading to a higher activity of Factor II and Factor X and in increased tendency to thrombosis.


An antithrombotic agent is a drug that reduces the formation of blood clots (thrombi). Antithrombotics can be used therapeutically for prevention (primary prevention, secondary prevention) or treatment of a dangerous blood clot (acute thrombus).


Argatroban is an anticoagulant that is a small molecule direct thrombin inhibitor. Argatroban was licensed by the Food and Drug Administration (FDA) for prophylaxis or treatment of thrombosis in patients with heparin-induced thrombocytopenia (HIT). It was also approved for use during percutaneous coronary interventions in patients who have HIT or are at risk for developing it.

Arterial thrombosis

Arterial thrombosis is the formation of a thrombus within an artery. In most cases, arterial thrombosis follows rupture of atheroma, and is therefore referred to asatherothrombosis.

Another common cause of arterial occlusion is atrial fibrillation, which causes a blood stasis within the atria with easy thrombus formation. In addition, it is well known that the direct current cardioversion of atrial fibrillation carries a great risk of thromboembolism, especially if persisting more than 48 hours. Thromboembolism strikes approximately 5% of cases not receiving anticoagulant therapy. When cardiac rhythm is restored clots are pushed out from atria to ventricles and from these to the aorta and its branches.

Arterial thrombosis can embolize and is a major cause of arterial embolism, potentially causing infarction of almost any organ in the body.


Arteries (from Greek ἀρτηρία (artēria), meaning “windpipe, artery”) are blood vessels that carry blood away from the heart. While most arteries carry oxygenated blood, there are two exceptions to this, the pulmonary and the umbilical arteries. The effective arterial blood volume is that extracellular fluid which fills the arterial system.

The circulatory system is vital for sustaining life. Its normal functioning is responsible for the delivery of oxygen andnutrients to all cells, as well as the removal of carbon dioxide and waste products, the maintenance of optimum pH, and the circulation of proteins and cells of the immune system. In developed countries, the two leading causes of death,myocardial infarction (heart attack), and stroke, may each directly result from an arterial system that has been slowly and progressively compromised by years of deterioration.


Aspirin (BAN, USAN), also known as acetylsalicylic acid [ASA], is a salicylate drug, often used as an analgesic to relieve minor aches and pains, as an antipyretic to reduce fever, and as an anti-inflammatory medication. Aspirin also has an antiplatelet effect by inhibiting the production of thromboxane, which under normal circumstances binds platelet molecules together to create a patch over damaged walls of blood vessels. Because the platelet patch can become too large and also block blood flow, locally and downstream, aspirin is also used long-term, at low doses, to help prevent heart attacks, strokes, and blood clot formation in people at high risk of developing blood clots. Also, low doses of aspirin may be given immediately after a heart attack to reduce the risk of another heart attack or of the death of cardiac tissue. Aspirin may be effective at preventing certain types of cancer, particularly colorectal cancer.

The main side effects of aspirin are gastrointestinal ulcers, stomach bleeding, and ringing in the ears, especially with higher doses. In children and adolescents, aspirin is not recommended for flu-like symptoms or viral illnesses, because of the risk of Reye’s syndrome.

Aspirin is part of a group of medications called nonsteroidal anti-inflammatory drugs (NSAIDs), but differs from most other NSAIDs in the mechanism of action. Though it and others with similar structure, called the salicylates, have similar effects (antipyretic, anti-inflammatory, analgesic) to the other NSAIDs and inhibit the same enzyme cyclooxygenase (COX), aspirin does so in an irreversible manner and, unlike others, affects more the COX-1 variant than the COX-2 variant of the enzyme.