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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Adenosine Diphosphate, Adult, Aged, Aged, 80 and over, Angioplasty, Balloon, Angioplasty, Balloon, Coronary, Arachidonic Acid, Aspirin, Case-Control Studies, Cell Adhesion Molecules, Clopidogrel, Drug Therapy, Combination, Female, Flow Cytometry, Humans, Lipopolysaccharide Receptors, Male, Microfilament Proteins, Middle Aged, Monocytes, P-Selectin, Phosphoproteins, Phosphorylation, Platelet Adhesiveness, Platelet Aggregation, Platelet Aggregation Inhibitors, Platelet Glycoprotein GPIb-IX Complex, Stents, Ticlopidine.
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Is the formation of monocyte-platelet aggregates independent of on-treatment residual agonists'-inducible platelet reactivity? Context: Circulating monocyte-platelet aggregates (MPA) are a sensitive marker of in vivo platelet activation and patients with atherosclerotic vascular disease exhibit higher levels of MPA. Clopidogrel has been shown to reduce MPA formation in these patients to a greater extent than aspirin. However, response to clopidogrel and aspirin shows a wide variability, and patients with high on-treatment residual platelet reactivity are at an increased risk for adverse events after coronary stenting. We therefore investigated the association of MPA with on-treatment residual agonists'-inducible platelet aggregation in 125 patients on dual antiplatelet therapy after peripheral, coronary or carotid artery stenting. MPA were characterized by co-expression of monocyte marker CD14 and platelet-specific markers (CD42b and CD62P) by whole blood flow cytometry. Platelet reactivity was determined by light transmission aggregometry, the VerifyNow P2Y12 and aspirin assays, and the vasodilator-stimulated phosphoprotein phosphorylation assay. Cut-off values for residual platelet reactivity were defined according to quartiles of each assay. The extent of MPA formation showed no significant differences between patients without and with residual ADP-inducible platelet reactivity, and between individuals without and with residual arachidonic acid (AA)-inducible platelet reactivity. Even patients with combined on-treatment residual ADP- and AA-inducible platelet reactivity did not exhibit significantly higher levels of MPA than patients without any on-treatment residual platelet reactivity.
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High on-treatment residual agonists'-inducible platelet reactivity results in less than a 25% increase in circulating MPA, suggesting that MPA formation is largely dependent on other factors. Final Decision: yes