3-OR: Differential Effects of Novel Antidiabetic Agents on Vascular Function Indices in Patients with Type 2 Diabetes Mellitus

Diabetes(2019)

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摘要
Background: Arterial stiffness is a well-established surrogate marker of vascular properties in patients with type 2 diabetes mellitus (DM2). We aimed to investigate whether optimization of DM2 therapy with novel antiglycemic agents additional to metformin, may improve arterial wall properties. Methods: We enrolled 99 consecutive patients (male gender=63.3%) receiving metformin and still not achieving the therapeutic targets. Subjects were assigned to age and sex matched equal groups (n=33/group) of an additional antiglycemic agent; either DPP-4i, SGLT2i (n=28) or GLP-1 agonists. Applanation tonometry was used to assess non-invasively augmentation index (AIx) and aortic pulse wave velocity (PWV) as a measure of arterial stiffness at baseline and at 3-month follow-up. Among other demographics data, hemoglobin A1c (HbA1c) was measured. Results: There was no difference for male gender (p=0.10) or age (64.92 ± 8.30 years, p=0.27) between the 3 study groups. Interestingly, baseline values improved significantly after SGLT2i and DPP-4i administration both for PWV (11.46 ± 2.77 vs. 9.83 ± 2.19 m/s and 10.89 ± 2.35 vs. 9.68 ± 1.77 m/s respectively, p=0.01 for both) and AIx (28.81 ± 8.55 vs. 25.82 ± 7.40 and 27.91 ± 13.05 vs. 24.91 ± 12.70 respectively, p=0.01 for both), when compared to those at follow-up time. In contrast, GLP-1A administration decreased PWV (12.82 ± 3.00 m/s at baseline vs. 11.67 ± 2.77 m/s during follow-up, p<0.001) but not AIx (31.64 ± 6.21 vs. 30.18 ± 6.03, p= 0.18). HbA1c at baseline was uniformly decreased in all study groups when compared to follow-up (7.52% vs. 6.72% for SGLT2i, 7.76% vs. 6.92% for DPP-4i and 8.19% vs. 6.85% for GLP-1A, p<0.001 for all). Conclusion: The optimization of DM2 treatment with SGLT2i, DPP-4i or GLP-1A, added to metformin, not only helps to achieve better glycemic control but significantly ameliorates arterial stiffness indices and achieves therapeutic targets in patients with DM2. Disclosure G. Siasos: None. E. Bletsa: None. P.K. Stampouloglou: None. K. Batzias: None. S.A. Paschou: None. A. Antonopoulos: None. V. Tsigkou: None. N. Gouliopoulos: None. S. Mazaris: None. E. Oikonomou: None. A. Thanopoulou: None. M. Politou: None. A. Vryonidou: None. D. Tousoulis: None. N. Tentolouris: None.
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