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Microfluidics in Assessing Platelet Function
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Fibrin clot structure and platelet aggregation in patients with aspirin treatment failure

Søs Neergaard-Petersen1, Ramzi Ajjan, Anne-Mette Hvas

  • 1Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark ; Division of Cardiovascular and Diabetes Research, Leeds Institute for Genetics, Health and Therapeutics, University of Leeds, Leeds, United Kingdom.

Plos One
|August 27, 2013
PubMed

Insights

Patients with aspirin treatment failure exhibit increased platelet aggregation and altered clot structure, indicating a higher risk of cardiovascular events. Measuring platelet function and clot characteristics may help identify this risk.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Pharmacology

Background:

  • Aspirin is crucial for preventing cardiovascular events by modulating platelet aggregation and fibrin clot formation.
  • Aspirin treatment failure (ATF) occurs when patients experience cardiovascular events despite aspirin therapy.
  • Understanding the mechanisms behind ATF is vital for improving patient outcomes.

Purpose of the Study:

  • To evaluate platelet aggregation and fibrin clot structure in patients with ATF.
  • To compare these parameters between patients with and without myocardial infarction (MI) while on aspirin therapy.
  • To identify potential biomarkers for predicting ATF.

Main Methods:

  • 177 stable coronary artery disease patients on aspirin monotherapy were included.
  • ATF was defined as myocardial infarction (MI) occurring during aspirin treatment (116 patients, 66%).
  • Platelet aggregation was assessed using Multiplate® and VerifyNow®; fibrin clot structure was analyzed via turbidimetric assays and scanning electron microscopy.

Main Results:

  • Patients with ATF showed significantly enhanced platelet aggregation in response to arachidonic acid and collagen.
  • Increased fibrin network density (clot maximum absorbance) and thinner fibers were observed in ATF patients.
  • ATF was associated with prolonged clot lysis time and elevated C-reactive protein (CRP) levels.

Conclusions:

  • Aspirin treatment failure is characterized by increased platelet aggregation and altered fibrin clot structure with impaired fibrinolysis.
  • These findings suggest that assessing platelet function and fibrin clot characteristics could help identify patients at increased risk of ATF.
  • This highlights potential avenues for personalized antiplatelet therapy strategies.
Abstract

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