Evaluation of the TEG® platelet mappingTM assay in blood donors

Louise Bochsen; Bo Wiinberg; Mads Jens Kjelgaard-Hansen; Daniel A. Steinbrüchel; Pär I. Johansson

doi:10.1186/1477-9560-5-3

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

Louise Bochsen, Bo Wiinberg, Mads Jens Kjelgaard-Hansen, Daniel A. Steinbrüchel, Pär I. Johansson

77 Citationer (Scopus)

719 Downloads (Pure)

Abstract

Background

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^TM 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.

Methods

In 43 healthy blood donors, the analytical (CV_a) and inter-individual variability (CV_g) of the TEG^®Platelet Mapping^TM assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP.

Results

The CV_aof the assay for maximal platelet contribution to clot strength (MA_Thrombin) was 3.5%, for the fibrin contribution to clot strength (MA_Fibrin) 5.2%, for MA_AA4.5% and for MA_ADPit was 6.6%. The MA_ThrombinCV_gwas 2.8%, MA_Fibrin4.7%, MA_AA6.6% and for MA_ADPit was 26.2%. Females had a higher MA_Thrombincompared 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).

Conclusion

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^®enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy.

Originalsprog	Engelsk
Tidsskrift	Thrombosis Journal
Vol/bind	5
Udgave nummer	3
Antal sider	5
ISSN	1477-9560
DOI	https://doi.org/10.1186/1477-9560-5-3
Status	Udgivet - 2007

Adgang til dokumentet

10.1186/1477-9560-5-3

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Citationsformater

@article{9573ecc0a1c311ddb6ae000ea68e967b,

title = "Evaluation of the TEG{\textregistered} platelet mappingTM assay in blood donors",

abstract = "BackgroundMonitoring 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{\textregistered} Platelet MappingTM 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.MethodsIn 43 healthy blood donors, the analytical (CVa) and inter-individual variability (CVg) of the TEG{\textregistered} Platelet MappingTM assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP.ResultsThe 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).ConclusionThe 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{\textregistered} enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy.",

author = "Louise Bochsen and Bo Wiinberg and Kjelgaard-Hansen, {Mads Jens} and Steinbr{\"u}chel, {Daniel A.} and Johansson, {P{\"a}r I.}",

year = "2007",

doi = "10.1186/1477-9560-5-3",

language = "English",

volume = "5",

journal = "Thrombosis Journal",

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publisher = "BioMed Central",

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TY - JOUR

T1 - Evaluation of the TEG® platelet mappingTM assay in blood donors

AU - Bochsen, Louise

AU - Wiinberg, Bo

AU - Kjelgaard-Hansen, Mads Jens

AU - Steinbrüchel, Daniel A.

AU - Johansson, Pär I.

PY - 2007

Y1 - 2007

N2 - BackgroundMonitoring 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 MappingTM 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.MethodsIn 43 healthy blood donors, the analytical (CVa) and inter-individual variability (CVg) of the TEG® Platelet MappingTM assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP.ResultsThe 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).ConclusionThe 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® enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy.

AB - BackgroundMonitoring 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 MappingTM 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.MethodsIn 43 healthy blood donors, the analytical (CVa) and inter-individual variability (CVg) of the TEG® Platelet MappingTM assay were determined together with platelet receptor inhibition in response to arachidonic acid (AA) and ADP.ResultsThe 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).ConclusionThe 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® enables, however, for routine monitoring of the variability in ADP receptor inhibition and of antiplatelet therapy.

U2 - 10.1186/1477-9560-5-3

DO - 10.1186/1477-9560-5-3

M3 - Journal article

SN - 1477-9560

VL - 5

JO - Thrombosis Journal

JF - Thrombosis Journal

IS - 3

ER -