The effect of DPP-4i, GLP-1RA, SGLT-2i and long-acting insulin on platelet function in patients with type 2 diabetes mellitus

Abstract Background Patients with type 2 diabetes mellitus (T2DM) are at higher risk for thrombotic events. Platelet function may be used to assess prothrombotic state in patients with cardiovascular disease. Purpose We aimed to investigate whether the administration of novel antidiabetic agents influence platelet function in TDM2 patients. Patients and methods We 60 enrolled consecutive patients with T2DM, on stable antidiabetic therapy, who did not achieve therapeutic targets. Subjects were assessed to receive an additional anti-diabetic agent; dipeptidyl peptidase-4 inhibitor (DPP4i, n=14), glucagon like peptide-1 receptor agonist (GLP1RA, n=24), sodium/glucose cotransporter-2 inhibitor (SGLT2i, n=22). Platelet reactivity was measured with PFA-200 collagen/epinephrine (c-EPI) and PFA-200 collagen/ADP (c-ADP) closure time. Glycosylated hemoglobin (HbA1c), c-EPI and c-ADP were assessed at baseline and 3 months after treatment intensification. Results There was no difference between the study groups regarding gender, age, hypertension, dyslipidemia, smoking, Hba1c and CADP or CEPI (p=NS for all) at baseline. All groups achieved better glycemic control in terms of HbA1c values between baseline and follow-up (for DPP4i: 7.4±0.2% vs 6.7±0.2%, for GLP1RA: 8.3±0.2% vs 6.9±0.1%, for SGLT2i: 7.5±0.1% vs 6.7±0.1% and for insulin 9.8±0.5% vs 7.7±0.4%, p<0.001 for all). After a 3 month-period, treatment intensification with these novel agents did not influence c-EPI and c-ADP values [155.4±6.64 sec vs 152.9±8.28 sec (p=0.678) and 106.6±4.30 sec vs 106.8±3.93 sec (p=0.955) respectively] in whole population. In subgroup analysis, for patients off antiplatelet treatment (n=31), c-EPI was significantly decreased from 148.4±8.5 to 129.8±13.9 sec (p=0.036), but not c-ADP (from 105.4±5.3 to 99.3±4.9 sec, p=0.094). In patients who did receive antiplatelets (n=37), c-EPI and c-ADP were not significantly changed (c-EPI 163.1±10.9 to 179.6±13.9 sec p=0.201 and c-ADP from 106.6±8.2 sec to 114.6±7.3 sec, p=0.318) respectively. Conclusion Antiplatelet treatment prevents thrombotic risk in T2DM patients receiving novel antidiabetics. The effects of novel antidiabetics on platelet reactivity -as well as any distinct class properties- merits further investigation. Acknowledgement/Funding None