Effects Of Novel Antidiabetic Therapy On Platelet Reactivity In Patients With Type 2 Diabetes Mellitus

Background: Patients with type 2 diabetes mellitus (DM2) exert a higher risk for thrombotic events. Platelet reactivity may be used to assess prothrombotic state in patients with cardiovascular disease. We aimed to investigate whether the administration of novel antiglycemic agents may influence platelet reactivity in these patients. Methods: We enrolled 99 patients (male=63.3%) receiving metformin for DM2 who did not achieve therapeutic targets under current treatment. Subjects were assigned to age and sex matched groups (n=33 per group) of an additional antiglycemic agent; either DPP-4 inhibitor, SGLT2 inhibitor or a GLP-1 agonist. Platelet reactivity was measured with PFA-200 assay; collagen/epinephrine (CEPI) and collagen/ADP closure time (CADP) were calculated in seconds and HbA1c at baseline and at 3 months. Results: There was no difference for male gender (p=0.10) or age (64.92 ± 8.30 years, p=0.27) between the study groups. All patients achieved better glycemic control in terms of HbA1c values between baseline and follow-up (7.78% vs. 6.92% for DPP-4, 7.52% vs. 6.73% for SGLT2 and 8.19% vs. 6.85% for GLP-1, p<0.001 for all). Platelet reactivity did not differ significantly at baseline between the study groups (p=0.71 for CEPI and p=0.6 for CADP). Additionally, CEPI (p=0.54) and CADP (p=0.43) did not change significantly at follow-up in all groups. Interestingly, when we conducted a separate analysis for patients not receiving antiplatelet agents, we observed that only CADP was significantly reduced at follow-up time after DPP-4 and GLP-1 treatment, but not after SGLT2 administration (148.50 ± 60.65 vs. 119.75 sec for DPP-4, p=0.01, 104.12 ± 25.68 vs.88.7 ± 22.25 sec for GLP-1, p=0.01 and 101.57 ± 15.26 vs. 88.57 ± 13.26 sec for SGLT2, p=0.73). Conclusion: The addition of DPP-4 or GLP-1 to metformin influences platelet reactivity and achieves better glycemic control in DM2 patients, providing further insights in the pathophysiology of DM2. Disclosure G. Siasos: None. E. Bletsa: None. P.K. Stampouloglou: None. K. Batzias: None. A. Antonopoulos: None. S.A. Paschou: None. V. Tsigkou: None. N. Gouliopoulos: None. S. Mazaris: None. G. Vogiatzi: None. S. Tsalamandris: None. E. Oikonomou: None. M. Zaromytidou: None. M. Politou: None. A. Vryonidou: None. A. Thanopoulou: None. N. Tentolouris: None. D. Tousoulis: None.