What is partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT)?

Updated: Jul 02, 2021
  • Author: Muhammad Bader Hammami, MD; Chief Editor: Eric B Staros, MD  more...
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Partial thromboplastin time (PTT) and activated partial thromboplastin time (aPTT) are used to test for the same functions; however, in aPTT, an activator is added that speeds up the clotting time and results in a narrower reference range. The aPTT is considered a more sensitive version of the PTT and is used to monitor the patient’s response to heparin therapy.

The aPTT test is used to measure and evaluate all the clotting factors of the intrinsic and common pathways of the clotting cascade by measuring the time (in seconds) it takes a clot to form after adding calcium and phospholipid emulsion to a plasma sample. The result is always compared to a control sample of normal blood.

The aPTT evaluates factors I (fibrinogen), II (prothrombin), V, VIII, IX, X, XI and XII. (A retrospective study by Bachler et al indicated that in critically ill patients, a factor XII level of 42.5% or less leads to spontaneous prolongation of aPTT.) [7]

When the aPTT test is performed in conjunction with prothrombin time (PT) test, which is used to evaluate the extrinsic and common pathways of the coagulation cascade, a further clarification of coagulation defects is possible. If, for example, both the PT and aPTT are prolonged, the defect is probably in the common clotting pathway, and a deficiency of factor I, II, V, or X is suggested. A normal PT with an abnormal aPTT means that the defect lies within the intrinsic pathway, and a deficiency of factor VIII, IX, X, or XIII is suggested. A normal aPTT with an abnormal PT means that the defect lies within the extrinsic pathway and suggests a possible factor VII deficiency. [1, 2, 6, 8]

Normal hemostasis

Normal hemostasis is achieved when there is a balance between factors that encourage clotting and factors that encourage clot dissolution. Following damage to a blood vessel, the first reaction of the body is vascular constriction to reduce blood loss. In small-vessel injury, this may be enough to stop bleeding. However, for large blood vessels, hemostasis is required.

Primary hemostasis occurs within seconds and results in platelet plug formation at sites of injury.Next, secondary hemostasis occurs, which consists of the reactions of the plasma coagulation system that result in fibrin formation. It requires several minutes for completion. The fibrin strands that are produced strengthen the primary hemostatic plug.

In the first phase of reactions, called the intrinsic system, 3 plasma proteins, Hageman factor (factor XII), high-molecular-weight kininogen, and prekallikrein, form a complex on vascular subendothelial collagen, and, through a series of reactions, activated factor XI (XIa) is formed and activates factor IX (IXa). Then, a calcium- and lipid-dependent complex is formed between factors VIII, IX, and X, and activated X (Xa) is formed.

At the same time, the extrinsic system is activated and provides a second pathway to initiate coagulation by activating factor VII (VIIa). In this pathway, a complex formed between factor VII, calcium, and tissue factor results in activation of factor VII (VIIa). VIIa can directly activate factor X and activated X (Xa) is formed. Alternatively, both factors IX and X can be activated more directly by factor VIIa, generated via the extrinsic pathway. Activation of factors IX and X provides a link between the intrinsic and extrinsic coagulation pathways.

The final step, the common pathway, converts prothrombin II to thrombin (IIa) in the presence of activated V (Va), activated X (Xa), calcium, and phospholipid. The main purpose of thrombin (IIa) is the conversion of fibrinogen to fibrin, which is then polymerized into an insoluble gel. The fibrin polymer is then stabilized by the cross-linking of fibrin polymers by factor XIII.

Clot lysis and vessel repair begin immediately after the formation of the definitive hemostatic plug. Three potential activators of the fibrinolytic system, Hageman factor fragments, urinary plasminogen activator, and tissue plasminogen activator, diffuse from endothelial cells and convert plasminogen, which had previously been adsorbed to the fibrin clot, into plasmin. Plasmin then degrades fibrin polymer into small fragments, which are cleared by the macrophages. [9]

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