Highlights
- •In the PFA–100® analyser, the shorter closure times (CT) are associated with an increased VTE risk.
- •Whole blood aggregation is not related to VTE risk.
- •Other mechanisms of platelet function, such as adhesion, must be involved in the pathogenesis of VTE.
Abstract
Introduction
Platelets play a role in the pathophysiology of venous thromboembolism (VTE). Some
studies have not found an association between VTE and platelet aggregation. The PFA–100®
analyser is an in vitro assay for assessing primary haemostasis. But, there are no studies to evaluate its
association with VTE. We investigated the contribution of the global platelet function
and aggregation in the development of VTE.
Material and methods
We analysed 800 individuals who were included in the RETROVE Study (Riesgo de Enfermedad
TROmboembólica VEnosa). Global platelet function was evaluated as closure times (CT)
with the agonists ADP and epinephrine using a PFA–100® analyser. Platelet aggregation
was evaluated by Multiplate™ analyser. The VTE risk for all the parameters was calculated
by unconditional logistic regression analyses considering the potential confounders:
age, gender, body mass index (BMI), factor VIII (FVIII), the von Willebrand factor
(vWF) and the ABO blood group system.
Results
The unadjusted odds ratio (OR) values ≤10th percentile for the PFAadp and PFAepi were 4.02 (95% CI, 2.76–5.95)
and 3.33 (2.27–4.97). Also, after adjusting for vWF, we obtained lower OR for the
PFAadp and for PFAepi: 2.24 (1.44–3.49) and 1.63 (1.04–2.59). But, the whole blood
aggregation parameters did not shown an association with VTE risk.
Conclusion
We demonstrated an association between short CT and VTE risk. Although, the whole
blood aggregation parameters did not show an association with the VTE risk. This striking
contrast suggests that there are other platelet function mechanisms (e.g. adhesion) that are responsible of VTE risk.
Keywords
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Article info
Publication history
Published online: July 12, 2018
Accepted:
July 5,
2018
Received in revised form:
June 27,
2018
Received:
April 20,
2018
Identification
Copyright
© 2018 Elsevier Ltd. All rights reserved.