Liv Vernstrøm1, Kristian Løkke Funck2, Erik Lerkevang Grove3, Esben Laugesen4, Jonathan Mathias Baier5, Anne-Mette Hvas6, Per Løgstrup Poulsen7. 1. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: lvh@clin.au.dk. 2. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: klf@clin.au.dk. 3. Department of Cardiology, Aarhus University Hospital, Aarhus, Denmark; Department of Clinical Medicine, Institute of Health, Aarhus University, Denmark. Electronic address: erikgrove@dadlnet.dk. 4. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: esben.laugesen@clin.au.dk. 5. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: baier@clin.au.dk. 6. Department of Clinical Medicine, Institute of Health, Aarhus University, Denmark; Department of Clinical Biochemistry, Centre of Haemophilia and Thrombosis, Aarhus University Hospital, Aarhus, Denmark. Electronic address: annehvas@rm.dk. 7. Department of Endocrinology and Internal Medicine, Aarhus University Hospital, Aarhus, Denmark. Electronic address: perpouls@rm.dk.
Abstract
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 1h after administration of 75mg of aspirin. Participants were then treated for 6days with once-daily aspirin, and blood sampling was repeated 1h and 24h after aspirin intake. RESULTS: After 6days 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.
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 1h after administration of 75mg of aspirin. Participants were then treated for 6days with once-daily aspirin, and blood sampling was repeated 1h and 24h after aspirin intake. RESULTS: After 6days 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.
Authors: William A E Parker; Christian Schulte; Temo Barwari; Fladia Phoenix; Sam M Pearson; Manuel Mayr; Peter J Grant; Robert F Storey; Ramzi A Ajjan Journal: Cardiovasc Diabetol Date: 2020-01-07 Impact factor: 9.951
Authors: Robert F Storey; Ramzi A Ajjan; William A E Parker; Rebecca Sagar; Zeyad Kurdee; Fladia Hawkins; Khalid M Naseem; Peter J Grant Journal: Cardiovasc Diabetol Date: 2021-12-17 Impact factor: 8.949