Key result
Antiplatelet therapy suppresses post-TKA platelet activation markers elevated in pulmonary embolism.
Observational
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Platelet activation markers (platelet-derived microparticles and P-selectin on activated platelets), chemokines (monocyte chemotactic peptide and regulated on activation normally T-cell expressed and secreted), and soluble markers (sP-selectin, sE-selectin, sVCAM-1, and sCD14) were measured and compared in patients with pulmonary embolism (PE). These substances are thought to participate in the pathogenesis of PE. Levels of all of the platelet activation markers, chemokines, and soluble markers were higher in the patients with PE than in normal controls. Levels of platelet activation markers were also significantly increased postoperatively after total knee arthroplasty. Anti-platelet therapy significantly inhibited the elevation of platelet activation markers after total knee arthroplasty. These findings suggest that antiplatelet therapy may be useful for PE-related interaction of platelets, leukocytes, and endothelial cells.
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Inami et al. (2003) conducted an observational in Pulmonary embolism. Pulmonary embolism / Anti-platelet therapy vs. Normal controls was evaluated on Levels of platelet activation markers, chemokines, and soluble markers. Platelet activation markers were elevated in pulmonary embolism patients versus controls, and their post-total knee arthroplasty elevation was significantly inhibited by antiplatelet therapy.
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