Antiplatelet effect of aspirin during 24 h in patients with type 2 diabetes without cardiovascular disease

Descarga: Antiplatelet effect of aspirin during 24 h in patients with type 2 diabetes without cardiovascular disease

Archivo: tromboembolia-arterial/cardiopatia/Thr Res 2018 Vernstrom-asp y diabetes.pdf

Introduction: The antiplatelet effect of low-dose aspirin in patients with type 2 diabetes (T2DM) without cardiovascular disease (CVD) has not been thoroughly explored. We investigated if  platelet aggregation increased during the standard 24-hour aspirin dosing interval in patients with T2DM compared to non-diabetic controls. Furthermore, we evaluated baseline platelet aggregation, the acute effects of aspirin on platelet aggregation and platelet turnover.

Materials and methods: We included 21 patients with T2DM and 21 age and sex-matched controls. Platelet aggregation was measured by impedance aggregometry (Multiplate® Analyzer) and markers of platelet turnover by flow cytometry (Sysmex® XE-5000). Blood samples were obtained at baseline and 1 h after administration of 75 mg of aspirin. Participants were then treated for 6 days with once-daily aspirin, and blood sampling was repeated 1 h and 24 h after aspirin intake.

Results: After 6 days of treatment, platelet aggregation levels increased during the 24-hour aspirin dosing interval in both patients and controls (p < 0.001) with no difference between patients and controls. At baseline, patients with diabetes had increased platelet aggregation compared to controls (p =0.03). Platelet aggregation was reduced after the first dose of aspirin and significantly further reduced after six days of treatment (p < 0.001). Patients with T2DM had numerically higher immature platelet count compared to controls (p =0.09), indicating an increased platelet turnover.

Conclusion: Patients with T2DM without a history of CVD and controls had increased platelet aggregation at the end of the standard 24-hour dosing interval of aspirin. Further, aspirin-naïve T2DM patients had increased platelet aggregation compared to controls.

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