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Platelet hyper-function in acute coronary syndromes.

Paul Harrison1, Ian Mackie, Anthony Mathur

  • 1Haemostasis Research Unit, Department of Haematology, University College London, UK. Paul.Harriosn@ndm.ox.ac.uk

Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis
|November 5, 2005
PubMed
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Platelet hyper-function and elevated von Willebrand factor levels were observed in myocardial infarction (MI) patients, potentially explaining reduced responsiveness to aspirin (ASA). This indicates a need for further investigation into platelet behavior in acute coronary syndromes.

Area of Science:

  • Cardiovascular Medicine
  • Hematology
  • Platelet Physiology

Background:

  • Previous research indicates shortened bleeding times in acute coronary syndromes, particularly myocardial infarction (MI).
  • Platelet hyper-function is a suspected contributor to these bleeding time alterations.

Purpose of the Study:

  • To investigate platelet hyper-function in patients presenting with acute chest pain using the PFA-100.
  • To assess platelet responsiveness to aspirin (ASA) in patients with MI, unstable angina (UA), and non-specific chest pain.

Main Methods:

  • Utilized the PFA-100 with collagen/adenosine diphosphate and collagen/epinephrine cartridges for platelet function testing.
  • Studied 78 patients with acute chest pain (classified as MI, UA, or non-specific chest pain) and 20 healthy controls.

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  • All patients received 300 mg aspirin (ASA) >2 hours before blood sample collection; controls were tested pre- and post-ASA.

    • Main Results:

    • MI patients exhibited significantly shorter collagen/adenosine diphosphate closure times compared to controls (P=0.0237).
    • Unstable angina patients showed significantly longer collagen/epinephrine closure times than controls (P<0.0001), suggesting ASA response, while MI patients did not show a significant difference.
    • Von Willebrand factor levels were significantly elevated in both UA and MI patients compared to controls (P<0.0001), and further elevated in MI versus UA patients (P<0.05).

    Conclusions:

    • Evidence suggests platelet hyper-function and elevated von Willebrand factor levels in MI patients.
    • These findings may explain the decreased responsiveness to aspirin observed in MI patients on the collagen/epinephrine cartridge.
    • Further research is warranted to explore the mechanisms and clinical implications of platelet dysfunction in acute coronary syndromes.