EYES2019 7th ESE Young Endocrinologists and Scientists (EYES) Meeting Oral Presentations (67 abstracts)
1First Department of Cardiology, Hippokration Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 2Blood Bank and Haemophilia Unit, Hippokration Hospital, Athens, Greece; 3Department of Laboratory Hematology, Hippokration Hospital, Athens, Greece; 4Diabetes Center, Second Department of Internal Medicine, Hippokration Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 5Department of Endocrinology and Diabetes, Hellenic Red Cross Hospital, Athens, Greece; 6First Department of Internal Medicine, Laiko Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece; 7Diabetes Center, First Department of Propaedeutic Internal Medicine, Laiko Hospital, Medical School, National and Kapodistrian University of Athens, Athens, Greece.
Background: Patients with type 2 diabetes (T2D) are at higher risk for thrombotic events and as a result cardiovascular disease. 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 anti-diabetic 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 1054±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, c-ADP and 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. Effects of novel antidiabetics on platelet reactivity -as well as any distinct class properties- merits further investigation.