Platelet Aggregation


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Subject: Platelet Aggregation

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  • Platelets participate in primary hemostasis by forming aggregates at the site of injury. In vivo the platelets are stimulated by chemical substances called agonists or by interaction with damaged endothelial surfaces in the presence of von Willebrand factor and collagen. These properties are used in vitro to study the change in optical density as the platelets aggregate under the effect of added agonists (ADP, collagen, epinephrine, arachidonic acid, thrombin). Ristocetin is used to assess binding to von Willebrand factor, as reflected in platelets' agglutination. The aggregometers are photo optical instruments that require platelet-rich plasma. The more advanced equipment can use whole blood and can also assess ATP release by chemiluminescence methodology, thereby better determining platelet functionality.

  • Normal range: decrease in optical density of ≥65% (represented by graphs waves generated by the aggregometer). The results are also interpreted in relation to the role of each agonist in platelet physiology. The normal response to various agonists of ATP release in chemiluminescence assays is measured in nanomoles and reported as normal or abnormal.


  • Platelet aggregation studies are indicated in patients with a bleeding diathesis, especially mucocutaneous bleeding (but without acquired thrombocytopenia), when a platelet defect or von Willebrand disease is suspected. By varying the amount of the ristocetin reagent, subtype 2B or platelet type of von Willebrand disease can be diagnosed preliminarily.


Causes of Decreased Values

  • Congenital conditions:

    • The prototype for a severe platelet defect (thrombocytopathy) is Glanzmann thrombasthenia, where there is no aggregation with any agonists but positive agglutination with ristocetin.

    • Storage pool disease Bernard-Soulier syndrome.

    • Abnormal response to ristocetin may be due to von Willebrand disease.

  • Acquired conditions:

    • Effect of drugs. Abnormalities in response to arachidonic acid reflect, in most cases, ingestion of aspirin or other NSAIDs

    • Myeloproliferative neoplasms and plasmacytic neoplasms with high globulins

    • Uremia


  • Because of the short functional viability of platelets, the assay must be initiated within 2 hours from blood collection and completed within 4 hours.

  • The blood must be kept at room temperature at all times.

  • Platelet activation during blood drawing, such as traumatic draws with initiation of clotting, makes the assay invalid. Pneumatic tubes for delivering the blood should not be used.

  • Lipemic or hemolyzed blood may affect the in vitro platelet response.

  • Assays cannot be performed in severely thrombocytopenic patients.

  • Platelet aggregation studies have not been standardized to test for aspirin or clopidogrel “resistance” or hyperaggregability.

  • Platelet aggregation studies are labor intensive and require highly skilled, experienced technicians.