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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, RESULTS. Meshes: Aged, Aspirin, Blood Platelets, Collagen, Cyclooxygenase 1, Cyclooxygenase Inhibitors, Drug Resistance, Erythrocytes, Female, Humans, Male, Middle Aged, Platelet Activation, Platelet Aggregation, Platelet-Rich Plasma, Serotonin, Thromboxane A2, Vascular Diseases.
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Are residual platelet thromboxane A2 and prothrombotic effects of erythrocytes important determinants of aspirin resistance in patients with vascular disease? Context: Permanent inactivation of cyclooxygenase-1 and inhibition of platelet thromboxane A(2) (TxA(2)) constitute the main mechanisms underlying the prevention of vascular disease by aspirin. We studied platelet TxA(2) synthesis and its impact on platelet reactivity and platelet-erythrocyte [platelet-rich plasma (PRP)-RBC] interactions in 533 aspirin-treated patients with vascular disease. Seventy aspirin-free and 16 aspirin-treated normal subjects were evaluated as controls. Collagen (1 mug mL(-1))-induced platelet activation ((14)C-5HT release) and recruitment (proaggregatory activity of cell-free releasates from activated platelets) were assessed in PRP, PRP + RBC, and whole blood (WB). TxA(2) was quantified in releasates from WB. Aspirin inhibited TxA(2) synthesis and platelet function in all patients, but to different degrees. Forty-two patients (8%) displayed partial (<95%) inhibition of TxA(2) relative to that of aspirin-free controls. They produced >3.5 ng mL(-1) TxA(2) and had higher platelet reactivity than 491 patients who had undetectable TxA(2) or produced residual TxA(2) (R-TxA(2); </=3.5 ng mL(-1)). Patients with R-TxA(2) were distributed into TxA(2) quartiles. Patients in the third and fourth quartiles had significantly elevated (14)C-5HT release in PRP, which was markedly amplified in PRP + RBC and WB. TxA(2) in the fourth quartile translated into increased platelet aggregation and recruitment. Significant correlations were found between R-TxA(2) and platelet hyperfunction.
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Biochemical markers (TxA(2) synthesis, (14)C-5HT release) and biological assays (platelet aggregation and recruitment) used to monitor the aspirin effect in a large population of patients presenting with vascular disease have evidenced the importance of R-TxA(2) and the prothrombotic effects of RBC in aspirin resistance. Final Decision: yes