From: Elizabeth M. Van Cott, M.D., and Michael Laposata, M.D., Ph.D., “Coagulation.” In: Jacobs DS et al, ed. The Laboratory Test Handbook, 5th Edition. Lexi-Comp, Cleveland, 2001; 327-358.
Related Information
Antithrombin
Hypercoagulation Panel
Platelet Aggregation
Synonyms Hypercoagulable State, Platelet Aggregation; Platelet Aggregation, Hypercoagulable State; Platelet Autoaggregation
Test Includes Evaluation for spontaneous aggregation, and aggregation in response to low concentrations of adenosine diphosphate (ADP), epinephrine, arachidonate, and collagen
Abstract Platelet hyperaggregation in response to platelet agonists, and/or spontaneous platelet aggregation (aggregation without a platelet agonist) has been described in association with hypercoagulability, including strokes, myocardial infarction, and less commonly venous thrombosis.
Patient Preparation Patients should not have aspirin (or any medication containing aspirin) for at least 7 days prior to testing. Nonsteroidal anti-inflammatory drugs or other platelet-inhibiting agents should also be avoided.
Specimen Platelet-rich plasma
Container Four to six blue top or plastic (sodium citrate) tubes
Collection Routine venipuncture. Immediately invert tubes gently at least 4 times to mix. Deliver tubes immediately to the laboratory at room temperature (platelets are activated at cold temperatures).
Storage Instructions Keep specimen at room temperature and perform test within 2 hours of collection. Do not refrigerate or freeze specimen.
Causes for Rejection Specimen received more than 2 hours after collection, specimen clotted, specimen received on ice
Turnaround Time Less than 1 day
Special Instructions Test usually must be scheduled in advance with the laboratory.
Reference Interval No spontaneous platelet aggregation and no hyperaggregation compared to a normal control. Normal newborns can have decreased aggregation compared to adults.1
Use Evaluation for excessive platelet aggregation may be useful in patients with evidence of unexplained hypercoagulability and normal values in the routine hypercoagulation test panel.
Limitations Subjective. Results are compared to a normal control. Variable results among patients and controls. Platelet-inhibiting medications interfere. Labor-intensive for the laboratory, therefore, not suitable for high volume clinical testing.
Methodology As described for platelet aggregation, except each platelet agonist is tested at multiple lower-than-usual concentrations. For example, instead of testing epinephrine only at 10 microM, it is tested at 10 microM, 5 microM, 1 microM, and 0.5 microM. No agonist is added to one aliquot to assess for spontaneous aggregation.
Additional Information Various medications can cause increased in vitro platelet aggregation. If a patient is found to have increased platelet aggregation in this assay, a careful review of prescribed, as well as over-the-counter medications, is indicated. An on-line literature search for each medication is often informative. Hyperaggregation has also been reported with myeloproliferative disorders. Hereditary hyperaggregation as a cause of hypercoagulability is not well characterized.
Footnotes
1. Michelson AD, “Platelet Function in the Newborn,”Semin Thromb Hemost, 1998, 24(6):507-12.
References
Mammen EF, “Sticky Platelet Syndrome,”Semin Thromb Hemost, 1999, 25(4):361-5.
Landolfi R, Marchioli R, and Patrono C, “Mechanisms of Bleeding and Thrombosis in Myeloproliferative Disorders,”Thromb Haemost, 1997, 78(1):617-21.
