Why the study?
It was unclear whether collagen-induced aggregation is more diagnostic than standard agonists (arachidonic acid or ADP) in patients receiving dual antiplatelet therapy or aspirin monotherapy after CABG.
Does dual antiplatelet therapy reduce collagen-induced platelet aggregation compared to aspirin monotherapy in patients after CABG?
Does dual antiplatelet therapy reduce collagen-induced platelet aggregation compared to aspirin monotherapy in patients after CABG?
Collagen-induced platelet aggregation is higher in patients on aspirin monotherapy compared to DAPT after CABG, suggesting traditional agonists may be insufficient for comprehensive monitoring of antiplatelet therapy.
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Collagen MEA may refine perioperative platelet monitoring in CABG; leaves open superiority over ADP/AA for therapy guidance.
Introduction: Multiple electrode aggregometry (MEA) is used to assess platelet function and reactivity. This method allows for monitoring of antiplatelet therapy in patients and is important in the preoperative and perioperative periods, especially in patients after coronary artery bypass grafting (CABG). Aim: The aim of this study was to evaluate whether collagen-induced aggregation is more diagnostic than standard agonists (arachidonic acid or ADP) in patients receiving dual antiplatelet therapy (DAPT) or aspirin monotherapy (AM) after CABG. Materials and methods: The study included 155 patients with multi-vessel coronary artery disease and after CABG who were on antiplatelet therapy (aspirin 75 mg/day and clopidogrel 75 mg/day or aspirin 150 mg/day). Platelet aggregation in the blood of CABG patients, in response to arachidonic acid (0.5 mmol/L), collagen (3.2 μg/mL) and ADP (6.4 μmol/L) was assessed using a Multiplate® analyser. Results: Platelet aggregation induced by collagen, ADP, and arachidonic acid was statistically significantly higher in AM patients compared to DAPT patients (p<0.03, p <0.0001 and p<0.0001, respectively). Furthermore, collagen-dependent platelet aggregation was only partly inhibited in both groups. Conclusions: The use of traditional platelet agonists, such as ADP or arachidonic acid, is not sufficient to monitor antiplatelet therapy. Studies should be supplemented with additional platelet activation factors, such as collagen, to identify other receptors that may be important for antiplatelet therapy in cardiac patients.
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Szymańska et al. (2022) studied this question.
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