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[Difficulties in evaluating the efficacy of antiplatelet therapy in clinical practice]

L I Buriachkovskaia, I A Uchitel', A V Sumarokov

    Terapevticheskii Arkhiv
    |June 23, 2009
    PubMed

    Insights

    High platelet reactivity is common in coronary artery disease (CAD) patients on antiplatelet therapy. Resistance to these drugs is linked to inflammation and erythrocyte factors, not just standard tests.

    Area of Science:

    • Cardiology
    • Hematology
    • Pharmacology

    Background:

    • Platelet activity is crucial in managing coronary artery disease (CAD).
    • Antiplatelet therapies like aspirin and clopidogrel are standard treatments for CAD.
    • Understanding resistance to these therapies is vital for optimizing patient outcomes.

    Purpose of the Study:

    • To evaluate changes in platelet activity in CAD patients treated with aspirin, clopidogrel, or both.
    • To determine the prevalence of resistance to antiplatelet treatment in CAD patients.
    • To explore factors associated with antiplatelet resistance and altered platelet function.

    Main Methods:

    • Studied 199 stable CAD patients receiving aspirin, clopidogrel, or dual therapy, plus a control group of 25 healthy volunteers.
    • Assessed platelet aggregation using light transmission (LTM) and mean size of aggregates (MSA).
    • Utilized scanning electron microscopy to analyze platelet shape, leukocyte-platelet aggregates (LPA), and erythrocyte-platelet aggregates (EPA); measured IL-6 and sVCAM levels.

    Main Results:

    • High platelet reactivity was observed in 59.8% of CAD patients, primarily detected by spontaneous and low-dose ADP-induced aggregation.
    • Light transmission (LTM) only identified increased platelet reactivity in 10.7% of patients.
    • Resistance to aspirin and clopidogrel was associated with platelet heterogeneity, inflammation markers (IL-6, sVCAM), and erythrocyte-platelet aggregates (EPA).
    • Hemorrhagic events in some patients correlated with significantly decreased platelet aggregation.

    Conclusions:

    • Antiplatelet therapy resistance in CAD is multifactorial, involving platelet heterogeneity, inflammation, and erythrocyte status.
    • Standard LTM is insufficient for identifying all patients resistant to antiplatelet drugs; spontaneous and low-dose ADP-induced aggregation are more sensitive measures.
    • Over-inhibition of platelet activity may increase the risk of bleeding complications.
    Abstract

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