aPTT is a functional test which assesses “intrinsic pathway” (prekalicreine, high molecular weight kininogen-HK factors XII, XI, IX, VIII) and “village” of coagulation (factors X, V, II, I).

In vivo, the contact system is involved when blood interacts with a foreign surface such as cardiopulmonary bypass. FXIIa zymogen first batch protein binds to negatively charged surfaces (kaolin, dextran sulfate, sulphatides), causing auto activation and action on substrates, FXI and prekallikrein, kallikrein formation and FXIa. Kallikrein cleaves HK release of bradykinin and kinin-free kininogen (HK enabled).

In vitro activation is achieved by adding a so-called “partial thromboplastin”, composed only of phospholipids (does not contain the protein or tissue factor, as in “Full thromboplastin” used to initiate clotting in PT) and a surfactant , silica, providing negatively charged surface contact activation pathway of coagulation. Then there was added calcium chloride and measuring the time, expressed in seconds, to the formation of the clot. Laboratory Specialists PTT test developers gave the name “intrinsic pathway” cascade of reactions triggered based on misperceptions that PTT clotting is initiated without adding any external factor. In fact, an external factor is involved in the initiation of clotting in TTP or negatively charged glass surface reaction tube. This activation “contact” may be potentiated by adding particles, such as silica, kaolin, ellagic acid, in what we refer to today as partial thromboplastin test “on”. Contact activation is a trick used by laboratory professionals to determine the functionality of several important factors intrinsic pathway in a test tube.

Deficiency or inhibition HK, prekallikrein and factor XII, XI, IX and VIII prolong aPTT with normal PT, while deficiencies of factors “common pathway” of coagulation (X, V, II, fibrinogen) can prolong aPTT and PT both .

aPTT is not influenced by the FVII deficiency or FXIIa.

Recommendations for testing

– detecting congenital or acquired deficiency of coagulation factors mentioned above; suspicion of hemophilia or von Willebrand disease.

Deficiency of factor XII, prekallikrein or HK accompanying clinical manifestations are not bleeding. On the other hand, about 95% of congenital bleeding syndromes are accompanied by aPTT prolongation.

Monitor the treatment with unfractionated heparin and thrombin inhibitors (hirudin, argatroban);

Рsuspicion  of inhibitor-specific or non-specific coagulation factor (ex. lupus anticoagulant).

Note: this is associated with lupus anticoagulant clinic tendency to thrombosis and no bleeding.

– To evaluate preoperative risk of bleeding.


 Normal-: 26-40s

therapeutic -interval: during heparin therapy: 1.5-2.5 times the control level.

Heparin potentiates the inhibitory effect of intravenous anti-thrombin on factors XII, XI, IX, X and II (an effect especially on factors Xa and thrombin). The anticoagulant effect occurs immediately. Because the half-life of heparin is 3 hours, blood sample for aPTT are taken 3 hours after or one hour before the administration of heparin.