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April 19, 2023Journal of Thrombosis and HaemostasisOpen Access

The rate of platelet activation determines thrombus size and structure at arterial shear

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Why the study?

Current platelet function tests measure end-point activation without accounting for the speed of activation, potentially missing vital metrics to characterize platelet reactivity.

Population

Normal population

Comparison

Platelet activation kinetics across agonists and individuals

Design

In vitro laboratory assay development and evaluation

Authors

JMJoanne L. MitchellJDJoanne L. DunsterUniversity of NottinghamNKNeline KriekUniversity of Reading

Discussion

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Overview

Incorporating kinetic metrics may refine platelet reactivity assessment; leaves open impact on antiplatelet personalization pending validation.

Structured PICO

P
Population
Ex vivo human blood model using peripheral blood from 143 fasting, healthy, aspirin-free donors aged 30 to 65 years, and 43 patients investigated for stable CAD (8 with no CAD and no T2DM; 25 with CAD and no T2DM; 10 with CAD and T2DM). Exclusion criteria: acute coronary syndrome in the past 12 months, taking P2Y12 inhibitors, anticoagulants, other metabolic dysfunctions, active or recent malignancy (<2 years), pregnancy, evidence of alcohol or drug misuse, and any underlying hematologic pathologies.
I
Intervention
Measurement of platelet activation kinetics using a bespoke real-time flow cytometry assay (Kinetx) to assess the rate of fibrinogen binding and P-selectin exposure over time in response to various agonists (ADP, CRP-XL, epinephrine, thrombin, TRAP-6, U46619).
O
Outcome
Rate of platelet activation (change in fibrinogen binding and P-selectin exposure over the first 3 minutes) and its correlation with maximal platelet activation, thrombus size, and thrombus structure.surrogate

The rate of platelet activation is a novel, independent metric of platelet reactivity that predicts thrombus size and density at arterial shear, offering a potential new target for antiplatelet therapy.

Cite This Study

Mitchell et al. (2023) studied this question.

synapsesocial.com/papers/6a73a23c9d09e2fbac279dbdhttps://doi.org/10.1016/j.jtha.2023.03.044
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Triple antiplatelet therapy for preventing vascular events: a systematic review and meta-analysis2010 · 48 citations
  2. 2Multiparameter phenotyping of platelet reactivity for stratification of human cohorts2021 · 28 citations
  3. 3The kinetics of αIIbβ3 activation determines the size and stability of thrombi in mice: implications for antiplatelet therapy2010 · 78 citations
  4. 4Impaired synthesis and action of antiaggregating cyclic nucleotides in platelets from obese subjects: possible role in platelet hyperactivation in obesity2004 · 57 citations
  5. 5Evidence that phospholipase C‐γ2 interacts with SLP‐76, Syk, Lyn, LAT and the Fc receptor γ‐chain after stimulation of the collagen receptor glycoprotein VI in human platelets1999 · 64 citations