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Platelet function tests in thrombotic cerebrovascular disorders.

S Uchiyama, M Takeuchi, M Osawa

    Stroke
    |July 1, 1983
    PubMed
    Summary

    Platelet function tests reveal distinct patterns in cerebrovascular disease (CVD). Thrombotic CVD shows enhanced platelet aggregation and activators, unlike cardiogenic embolism, suggesting different disease mechanisms.

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    Area of Science:

    • Neuroscience
    • Hematology
    • Cardiology

    Background:

    • Obstructive cerebrovascular disease (CVD) encompasses various conditions, including transient ischemic attacks (TIA), reversible ischemic neurological deficits (RIND), and cerebral infarcts.
    • Cardiogenic embolism, often associated with rheumatic valvular heart disease (RVHD), represents a distinct cause of stroke.
    • Understanding platelet function is crucial for differentiating CVD subtypes and their pathogenesis.

    Purpose of the Study:

    • To investigate and compare platelet function in patients with different forms of obstructive cerebrovascular disease (CVD).
    • To evaluate the role of platelet aggregation, von Willebrand factor (VIII:vWF), platelet aggregation enhancing factor (PAEF), and megathrombocytes in CVD pathogenesis.
    • To assess the effect of aspirin therapy on platelet function in these patients.

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    Main Methods:

    • Platelet function tests including ADP and ristocetin-induced aggregation, spontaneous aggregation, VIII:vWF, PAEF, and percentage of large platelets (megathrombocytes) were performed.
    • Serial testing was conducted in acute stroke patients.
    • The impact of aspirin therapy (600 mg p.o.) on platelet parameters was examined.

    Main Results:

    • Patients with TIA, RIND, and cerebral infarct exhibited enhanced platelet aggregation (induced and spontaneous), elevated plasma VIII:vWF and PAEF, and increased megathrombocytes.
    • Patients with cardiogenic embolism showed normal results except for an increased percentage of megathrombocytes compared to non-embolic RVHD patients.
    • Platelet aggregation and megathrombocyte percentage increased slowly post-stroke and normalized with aspirin treatment.

    Conclusions:

    • A systemic increase in hyperaggregable platelets and plasma activators is associated with thrombotic CVD, potentially contributing to its pathogenesis.
    • Local hemodynamic factors may play a more significant role in the thrombogenesis of cardiogenic embolism.
    • Platelet function abnormalities in thrombotic CVD can be modulated by aspirin therapy.