Evaluation of the TEG® platelet mapping™ assay in blood donors

Department of Clinical Immunology, Rigshospitalet, University of Copenhagen, Copenhagen, DK-2100, Denmark.
Thrombosis Journal (Impact Factor: 1.31). 02/2007; 5(1):3. DOI: 10.1186/1477-9560-5-3
Source: PubMed


Monitoring of antiplatelet therapy in patients at cardiovascular risk is difficult because existing platelet function tests are too sophisticated for clinical routine. The whole blood TEG Platelet Mapping assay measures clot strength as maximal amplitude (MA) and enables for quantification of platelet function, including the contribution of the adenosine diphosphate (ADP) and thromboxane A2 (TxA2) receptors to clot formation.
In 43 healthy blood donors, the analytical (CVa) and inter-individual variability (CVg) of the TEG Platelet Mapping assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP.
The CVa of the assay for maximal platelet contribution to clot strength (MAThrombin) was 3.5%, for the fibrin contribution to clot strength (MAFibrin) 5.2%, for MAAA 4.5% and for MAADP it was 6.6%. The MAThrombin CVg was 2.8%, MAFibrin 4.7%, MAAA 6.6% and for MAADP it was 26.2%. Females had a higher MAThrombin compared to males (62.8 vs. 58.4 mm, p = 0.005). The platelet TxA2 receptor inhibition was 1.2% (range 0-10%) and lower than for the ADP receptor (18.6% (0-58%); p < 0.0001).
The high variability in ADP receptor inhibition may explain both the differences in response to ADP receptor inhibitor therapy and why major bleeding sometimes develops during surgery in patients not treated with ADP receptor inhibitors. An analytical variation of ~5 % for the TEG(R) enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy.

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