The analytical variation (CVa
) of the TEG®
Platelet Mapping™ assay was ~5% in alignment with the findings of Craft et al. [9
] investigating 120 subjects and concluding that this point of care assay makes it possible to conduct large scale comparative studies on the degree of platelet inhibition and patient outcome. Conventional aggregometry, representing the current "gold standard" for measuring platelet reactivity to ADP and AA and to assess the effect of antiplatelet agents, is valuable for the experienced and specialised laboratory.
The low analytical variation of the TEG®
Platelet Mapping™ assay found in this study may reflect the use of whole blood, obviating pre-analytical and analytic factors such as platelet count and size, preparation of platelet rich plasma (PRP), including centrifugation steps [11
]. The platelet function analyzer 100 (PFA-100), likely the most widely used point of care test for platelet inhibition, measures the time required for blood under simulated high shear flow to occlude a collagen/epinephrine or a collagen/ADP-coated aperture inserted in a plastic membrane. The PFA-100 is valuable for evaluation of platelet inhibition due to AA, while platelet inhibition due to ADP remains unsolved [13
]. Duplicate testing, however, is a requirement to obtain reliable results [14
The thrombin induced clot formation, MAThrombin
, represents the maximum uninhibited platelet function and was within the normal reference values of 51 to 69 mm, as described by the manufacturer, except for one donor having a MAThrombin
of 70.1 mm. A gender difference, with females having the higher MAThrombin
, suggests that females are better protected against bleeding than males [15
The TEG® Platelet Mapping™ assay enables for evaluation of the respective contribution of the ADP and the TxA2 receptors to clot formation by the addition of the appropriate agonists.
The response in platelet aggregation due to the agonist AA presented as the percentage inhibition of the platelet TxA2 receptor was less than 2% with no difference between gender and lower than the reported value of 14% [8
]. However, Gurbel et al. [8
] investigated only 6 donors, whereas 43 donors were evaluated in the present study. Genetic polymorphism in the platelet receptors has been reported and we cannot exclude that other differences exist between the two populations.
The variation in platelet aggregation due to ADP stimulation, evaluated as the percentage ADP receptor inhibition, was almost 60% and independent of gender. The inter-individual difference could be attributed to differences in the ADP receptors and to the number of receptors the individual possesses, varying the levels of ADP release, or platelet activation via alternative pathways [6
]. Differences in response to ADP receptor inhibitors between individuals have been demonstrated [16
] and may, at least in part, be due to the difference in platelet reactivity.
Patients treated with the ADP receptor inhibitor clopidogrel are at risk of major bleeding during surgery [18
]. Due to the high variation between the donors in ADP receptor inhibition, those with a high natural inhibition may be at risk of developing excessive bleeding during surgery.
Platelet Mapping™ assay enables relating the percent platelet inhibition to the individual's maximum uninhibited platelet function. Hereby the individual response to antiplatelet therapy is related to their own maximum uninhibited platelet function of potential therapeutic consequence. A MAThrombin
value above the normal reference range is associated with an increased risk of thrombotic complications and ischemic events [19
] implying that individual antiplatelet therapy may reduce the risk of recurrent events and also prevent the risk of bleeding.
Only Caucasian blood donors were studied and the utility of the assay for patients at cardiovascular risk remains to be evaluated. Natural platelet receptor inhibition was investigated and, therefore, the validity of the assay for monitoring patients in antiplatelet therapy was not assessed.