Platelet aggregation is important in hemostasis. A clump of platelets surrounds an area of acute blood vessel endothelial injury. Normal platelets adhere to this area of injury, and through a series of chemical reactions, they attract other platelets to the area. This is platelet aggregation, the first step in hemostasis. After this step the normal coagulation factor cascade occurs. Certain diseases that affect either platelet number or function can inhibit platelet aggregation and thereby prolong bleeding times. Congenital syndromes, uremia, myeloproliferative disorders, and drugs are associated with abnormal platelet aggregation. If blood is passed through a heart-lung or dialysis pump, platelet injury can occur and aggregation capability can be reduced.
Many agonists are used to stimulate platelet aggregation in the laboratory. Platelet aggregation is measured by determining the turbidity of platelet-rich plasma. As platelet aggregation is stimulated in vitro, turbidity decreases and light transmission through the specimen increases. This test is performed with an optical device called an aggregometer. Usually the patient’s blood specimen is spun to a platelet-rich component. Next, an agonist to platelet aggregation, such as adenosine diphosphate, collagen, epinephrine, or ristocetin, is added. Turbidity is then measured within the aggregometer, and a curve indicating light transmission per unit of time is plotted. Normal curves have been identified for any one agonist that is used.
This is a very sensitive test, and it can be significantly affected by a number of variables, including:
- Concentration of sodium citrate
- Platelet count
- Storage temperature
- Concentration of the agonist addition
- Reaction temperature
- Degrees of lipemia, hemoglobinemia, or bilirubinemia.
Causes of False Platelet Aggregation Test Resutls
It is very important to find out if the patient is receiving any drugs that may interfere with platelet aggregation or if the patient has any diseases such as jaundice, hyperlipidemia, or hemolysis and put that in consideration when the test results are looked at. The following are the factors and drugs that may cause false results to be seen:
- Factors that may cause increased platelet aggregation include blood storage temperature, hyperbilirubinemia, hemoglobinemia, hyperlipidemia, and platelet count.
- Drugs that may cause decreased platelet aggregation include antiplatelet drugs (e.g., ticlodipine), aspirin, some antibiotics, beta blockers, clofibrate, dextran, ethanol, heparin, Nonsteroidal Antiinflammatory Drugs (NSAIDs), phenothiazines, tricyclics, theophylline, and warfarin sodium (Coumadin).
Causes of Prolonged Platelet Aggregation
- Various congenital disorders including Wiskott-Aldrich Syndrome, Bernard-Soulier Syndrome, and Von Willebrand Disease: Platelet aggregation is diminished in autosomal recessive diseases.
- Connective Tissue Disorders including Lupus Erythematosus: The pathophysiology of these observations is not understood.
- Recent Cardiopulmonary or Dialysis Bypass: Platelet injury develops as the platelets are passing through this machinery. The injured platelets are less likely to function normally in regard to aggregation.
- Uremia: Not only is there a reduced platelet number in uremic patients, but a reduced aggregation capability has also been observed.
- Various Myeloproliferative diseases, including Leukemia, Myeloma, and Dysproteinemia: The pathophysiology of these observations is not clear. It may be related to abnormal antibodies affecting the platelet membrane.
- Drugs including Aspirin and Nonsteroidal Antiinflammatory Drugs (NSAIDs): Drugs can have an immediate, and in some cases long-lasting, negative effect on platelet aggregation.