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

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Abstract
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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Thrombosis Journal
Open Access
Original clinical investigation
Evaluation of the TEG
®
platelet mapping™ assay in blood donors
Louise Bochsen*
1
, Bo Wiinberg
2
, Mads Kjelgaard-Hansen
2
,
Daniel A Steinbrüchel
3
and Pär I Johansson
1
Address:
1
Department of Clinical Immunology, Rigshospitalet, University of Copenhagen, Copenhagen, DK-2100, Denmark,
2
Department of
Small Animal Clinical Sciences, The Small Animal Hospital, Faculty of Life Sciences, University of Copenhagen, Frederiksberg, DK-1870, Denmark
and
3
Department of Cardiothoracic Surgery, Rigshospitalet, University of Copenhagen, Copenhagen, DK-2100, Denmark
Email: Louise Bochsen* - louise.bochsen@rh.regionh.dk; Bo Wiinberg - bwi@life.ku.dk; Mads Kjelgaard-Hansen - mjkh@life.ku.dk;
Daniel A Steinbrüchel - daniel.steinbruchel@rh.regionh.dk; Pär I Johansson - per.johansson@rh.regionh.dk
* Corresponding author
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™ 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™ assay were determined together with platelet receptor inhibition in
response to arachidonic acid (AA) and ADP.
Results: The CV
a
of 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
AA
4.5% and for MA
ADP
it was
6.6%. The MA
Thrombin
CV
g
was 2.8%, MA
Fibrin
4.7%, MA
AA
6.6% and for MA
ADP
it was 26.2%. Females
had a higher MA
Thrombin
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).
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.
Background
Antiplatelet therapy is important for cardiovascular medi-
cine. The efficacy of aspirin in both primary and second-
ary prevention of myocardial infarction and stroke and
hence cardiovascular death is established [1,2] and the
addition of a platelet adenosine diphosphate (ADP)
receptor inhibitor, clopidogrel, further reduces these risks
[3,4]. Yet, platelet function tests (PFT) demonstrate that
subgroups of patients fail to develop the anticipated
antiplatelet effect of aspirin and/or clopidogrel [5,6]. The
PFT are, however, not applicable for routine purposes and
hence for clinical monitoring of antiplatelet therapy [7].
Published: 20 February 2007
Thrombosis Journal 2007, 5:3 doi:10.1186/1477-9560-5-3
Received: 7 September 2006
Accepted: 20 February 2007
This article is available from: http://www.thrombosisjournal.com/content/5/1/3
© 2007 Bochsen et al; licensee BioMed Central Ltd.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0
),
which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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Thrombosis Journal 2007, 5:3 http://www.thrombosisjournal.com/content/5/1/3
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The whole blood Thrombelastograph (TEG
®
) Platelet
Mapping™ assay measures clot strength, maximal ampli-
tude (MA), reflecting maximal platelet function, and
detects the reduction in platelet function, presented as
percentage inhibition, by both aspirin [8] and clopidog-
rel. This study evaluated the analytical (CV
a
) and inter-
individual (CV
g
) variation of the assay and the platelet
aggregation response, expressed as inhibition, to arachi-
donic acid (AA), representing a measure of the cyclooxy-
genase-1 (COX-1) activity, and to ADP in healthy blood
donors.
Methods
The study was in accordance with the Helsinki 2 Declara-
tion and the participants provided informed consent prior
to any study related activity. Forty-three Danish blood
donors, not taking any medication 10 days prior to the
investigation were included in the study. Blood was
drawn in citrate (9 volumes of blood into 1 volume of
0.129 M citrate, Vacutainer system, BD Biosciences, Ply-
moth, UK) and into heparin (17 IU/ml blood, Vacutainer
system, BD Biosciences, Plymoth, UK).
Thrombelastography
The TEG
®
Platelet Mapping™ assay (Haemoscope Corpo-
ration, Niles, Illinois, US) relies on evaluation of clot
strength to enable a quantitative analysis of platelet func-
tion. The maximal haemostatic activity is measured by a
kaolin activated whole blood sample treated with citrate.
The following measurements are performed with heparin
to eliminate thrombin activity: Reptilase and Factor XIII
(Activator F) generate a cross-linked fibrin clot to isolate
the fibrin contribution to the clot strength [9]. The contri-
bution of the ADP or ThromboxaneA2 (TxA2) receptors to
the clot formation is provided by the addition of ADP or
AA.
Blood was analyzed according to instructions (Haemo-
scope Corporation. TEG Guide to Platelet Mapping. Mon-
itor anti-platelet therapy, 2004). Both analyzer (series
5000) and the reagents were from Haemoscope Corpora-
tion.
For maximal clot strength (MA
Thrombin
) one milliliter of cit-
rate-stabilized blood was transferred to a vial containing
kaolin and mixed by inversion. Kaolin activated blood
(340 μl) was added to a TEG
®
cup containing 20 μl of 0.2
M CaCl
2
. To generate a whole-blood fibrin cross-linked
clot, representing only the fibrin contribution included in
the clot strength measurement, heparinized blood (360
μl) was transferred to a TEG
®
cup containing 10 μl Activa-
tor F; MA
Fibrin
(Fig. 1). The contribution of the P2Y12
receptor, or the COX-1 pathway, to the clot formation is
assessed by the addition of ADP or AA. Therefore, AA and
ADP, respectively, are added to Activator F to measure the
degree of ADP receptor and thromboxane A2 induced
platelet aggregation. Heparinized blood (360 μl) was
added to a TEG
®
cup in the presence of the Activator F and
agonist, 10 μl ADP (2 μM, final concentration) yielding
MA
ADP
or 10 μl AA (1 mM, final concentration) for the
MA
AA
. The platelet inhibition in response to the agonist is
calculated from platelet aggregation: [(MA
ADP
- MA
Fibrin
)/
(MA
Thrombin
- MA
Fibrin
) × 100] and % inhibition = (100% -
% aggregation).
Statistical analysis
The coefficient of variation for CV
a
and CV
g
was calculated
for MA
Thrombin
, MA
Fibrin,
MA
AA
and MA
ADP
[10]. Data are pre-
sented as mean ± SD or as mean with range. Comparisons
were made by Wilcoxon rank sum tests and a p-value <
0.05 was considered statistically significant.
Results
The MA
Thrombin
was 60.9 ± 5.3 mm (Table 1). When com-
paring genders, females had both the higher MA
Thrombin
and MA
Fibrin
(62.8 vs.58.3 mm, p = 0.005 and 8.1 vs. 6.6
mm; p = 0.035, respectively). The platelet aggregation in
response to AA, expressed as the percentage of natural
inhibition of the TxA2 receptor, varied between 0 and
10% with an average of 1.2%. The platelet aggregation in
response to ADP, expressed as the percentage of natural
inhibition of the ADP receptor, varied between 0 and 58%
with an average of 18.6% being higher than for the TxA2
receptor, p < 0.0001. No significant difference was, how-
ever, found between genders with regard to inhibition of
the TxA2 (1.3 vs. 1.1%, p = 0.71) or ADP receptors (18.2
vs. 19.4%, p = 0.41).
The CV
a
values were 3.5% for MA
Thrombin
, for MA
Fibrin
it was
5.2%, for MA
ADP
6.6 %, and for MA
AA
4.5%. The CV
g
for
MA
Thrombin
was 2.8%, for MA
Fibrin
it was 4.7% and for MA
AA
6.6%, whereas the CV
g
for the MA
ADP
was 26.2% (Table 2).
Discussion
The analytical variation (CV
a
) of the TEG
®
Platelet Map-
ping™ 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 aggregom-
etry, representing the current "gold standard" for measur-
ing 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 Map-
ping™ 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 [11,12]. The
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platelet function analyzer 100 (PFA-100), likely the most
widely used point of care test for platelet inhibition, meas-
ures the time required for blood under simulated high
shear flow to occlude a collagen/epinephrine or a colla-
gen/ADP-coated aperture inserted in a plastic membrane.
The PFA-100 is valuable for evaluation of platelet inhibi-
tion due to AA, while platelet inhibition due to ADP
remains unsolved [13,14]. Duplicate testing, however, is a
requirement to obtain reliable results [14].
The thrombin induced clot formation, MA
Thrombin
, repre-
sents 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 hav-
ing a MA
Thrombin
of 70.1 mm. A gender difference, with
females having the higher MA
Thrombin
, 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 appro-
priate 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 gen-
der and lower than the reported value of 14% [8]. How-
ever, 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 stimula-
tion, evaluated as the percentage ADP receptor inhibition,
Table 1: TEG
®
Platelet Mapping™ assay variables (see text) and percent platelet receptor inhibition for healthy blood donors.
All donors Females (n = 27) Males (n = 16)
MA
Thrombin
60.9 (4.5) 62.8 (5.3) 58.4 (5.4) *
MA
Fibrin
7.5 (2.7) 8.1 (2.8) 6.6 (2.2) *
MA
ADP
51.1 (8.1) 52.7 (7.8) 48.5 (8.1)
MA
AA
64.6 (4.7) 66.1 (4.5) 62.5 (4.3)
% ADP RI
a
18.6 (0–58.1) 18.2 (0–58.1) 19.4 (0–37.5)
% TxA2 RI
a
1.2 (0–10.1) 1.3 (0–9.8) 1.1 (0–10.1)
Values are mean and SD or range
a
RI = receptor inhibition
*Comparison between female and male donors, p < 0.05
Profiles of the TEG
®
Platelet Mapping™ assay parameters MA
Thrombin
, MA
ADP/AA
, and MA
Fibrin
Figure 1
Profiles of the TEG
®
Platelet Mapping™ assay parameters MA
Thrombin
, MA
ADP/AA
, and MA
Fibrin
.
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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]. Differ-
ences in response to ADP receptor inhibitors between
individuals have been demonstrated [16,17] and may, at
least in part, be due to the difference in platelet reactivity.
Patients treated with the ADP receptor inhibitor clopidog-
rel 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.
The TEG
®
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 ther-
apeutic consequence. A MA
Thrombin
value above the normal
reference range is associated with an increased risk of
thrombotic complications and ischemic events [19,20]
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.
Conclusion
An analytical variation of ~5 % for the TEG
®
Platelet Map-
ping™ assay enables for routine monitoring of antiplatelet
therapy in patients at cardiovascular risk. The high natural
ADP receptor variability may, in part, explain differences
in response to clopidogrel therapy. Furthermore, the high
variability in natural ADP receptor inhibition may explain
why unexpected bleeding can develop during surgery in
some patients as although they are not treated with ADP
receptor inhibitors.
Competing interests
The author(s) declare that they have no competing inter-
ests.
Authors' contributions
LB did all laboratory work, data collection and calculation
and contributed in the study design and manuscript prep-
aration. BW, MKH, DAS and PIJ were involved in the sta-
tistical analyses and contributed all to the preparation of
the manuscript. Additionally, PIJ participated in the
design of the study. All authors read and approved the
final manuscript.
Acknowledgements
Haemoscope Corporation, Niles, IL is acknowledged for support.
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) and inter-individual (CV
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®
Platelet Mapping™ assay variables (see text) in blood
donors.
MA
Thrombin
MA
Fibrin
MA
ADP
MA
AA
CV
a
(%) 3.5 5.2 6.6 4.5
CV
g
(%) 2.8 4.7 26.2 6.6
Page 4
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Page 5
    • "We found frequent (more than 75% of patients) and severe qualitative platelet dysfunction on TEG ® –PM in our patient cohort. The platelet dysfunction found on TEG ® –PM measures in our patient cohort was more pronounced compared to the routine TEG ® –PM evaluation of healthy adults and children with congenital heart defect before cardiopulmonary bypass (CPB) (13, 19 ). The qualitative platelet dysfunction was more common and pronounced to ADP-mediated aggregation compared to AA-mediated aggregation . "
    [Show abstract] [Hide abstract] ABSTRACT: Background: Bleeding complications are common and decrease the odds of survival in children supported with extracorporeal membrane oxygenation (ECMO). The role of platelet dysfunction on ECMO-induced coagulopathy and resultant bleeding complications is not well understood. The primary objective of this pilot study was to determine the incidence and magnitude of platelet dysfunction according to thromboelastography (TEG(®))-platelet mapping (PM) testing. Methods: Retrospective chart review of children <18 years old who required ECMO at a tertiary level hospital. We collected TEG(®)-PM and conventional coagulation tests data. We also collected demographic, medications, blood products administered, and clinical outcome data. We defined severe platelet dysfunction as <50% aggregation in response to an agonist. Results: We identified 24 out of 46 children on ECMO, who had TEG(®)-PM performed during the study period. We found the incidence of severe bleeding was 42% and mortality was 54% in our study cohort. In all samples measured, severe qualitative platelet dysfunction was more common for adenosine diphosphate (ADP)-mediated aggregation (92%) compared to arachidonic acid (AA)-mediated aggregation (75%) (p = 0.001). Also, ADP-mediated percent of platelet aggregation was significant lower than AA-mediated platelet aggregation [15% (interquartile range, IQR 2.8-48) vs. 49% (IQR 22-82.5), p < 0.001]. There was no difference in kaolin-activated heparinase TEG(®) parameters between the bleeding group and the non-bleeding group. Only absolute platelet count and TEG(®)-PM had increased predictive value on receiver operating characteristics analyses for severe bleeding and mortality compared to activated clotting time. Conclusion: We found frequent and severe qualitative platelet dysfunction on TEG(®)-PM testing in children on ECMO. Larger studies are needed to determine if the assessment of qualitative platelet function by TEG(®)-PM can improve prediction of bleeding complications for children on ECMO.
    Full-text · Article · Jan 2016
    • "In the area of cardiology, the use of TEG has expanded into monitoring of patients on antithrombotic therapy, such as GP IIb/IIIa antagonists or aspirin [1,11]. Given the immense variability in ADP receptor expression through the species , TEG is particularly useful in patients who appear to be " non-responders " to anti-thrombotic therapy as it permits ex vivo optimization of treatment [11,12]. The platelet mapping assay, a modification of TEG using some of the reagents inTable 1 , may be useful for predicting blood loss in patients who underwent CPB [13]. "
    [Show abstract] [Hide abstract] ABSTRACT: Analyzing coagulability often hinges on patient surveillance using prothrombin time (PT) or international normalized ratio (INR) and activated partial thromboplastin time (aPTT) to monitor the extrinsic and intrinsic coagulation pathways, respectively A more complete assessment, however, can often be obtained using thromboelastography (TEG), a coagulation assay that evaluates the efficiency of clot formation, as well as the viscoelastic properties of the clot. Developed by Dr. Helmut Hartert in 1948 at the University of Heidelberg, it provides information regarding hemostasis as a dynamic process [1,2]. Here, the TEG technique will be described, as well as its current applications and future directions for its use.
    Full-text · Article · Jan 2013
    • "The INR, aPTT, and platelet counts were performed in the hospital central laboratory. TEG and TEG Platelet Mapping (TEG/PM) Platelet function was determined using the TEG plateletmapping assay (Haemonetics, Niles, IL) [27] . A heparinized blood sample was collected and 360 ll of the blood sample was placed into pre-warmed cups of the TEG analyzer, followed by 10 ll of the prepared activator solution, comprised reptilase, factor XIIIa, and phospholipids (Haemonetics, Niles, IL). "
    Full-text · Article · Sep 2012
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