2357-PUB: Dapagliflozin for 52 Weeks Improves Diastolic Dysfunction and Vascular Reactivity in T2D
2019
Background: SGLT2i proved efficacy in reducing cardiovascular morbidity and mortality in T2D patients at high cardiovascular risk. Aims: In real-word setting, we prospectively evaluated long-term effects of Dapagliflozin (DAPA) on left diastolic ventricular function (LDVF) and vascular reactivity in T2D patients without known cardiovascular disease. Population, Study and Methods: 13 patients (9 male, 57± 8 years, BMI 29.6± 3.6, HbA1c 8.9±1.2%, years of T2D 9±5, fasting glucose 185±51 mg/dl) initiated DAPA 10 mg daily as add-on to metformin. Following data were collected at baseline (T0), after 12 weeks (T1) and 52 weeks (T2) of treatment: blood pressure, anthropometrics, fasting glucose, HbA1c, eGFR and lipids. Ratio of the early (E) to late (A) ventricular filling velocities (E/A) was used to evaluate LDVF. Arterial stiffness was evaluated by Pulse Wave Velocity (PWV) and Augmentation Index (AIxHR75) with radial approach (SphygmoCor System). Endothelial function was assessed by non-invasive flow mediated dilatation (FMD). Results: We observed significant percent variation in HbA1c (T1 vs. T0 -17.9%, p=0.001; T2 vs. T0 -17.4%, p=0.01), fasting glucose (T1 vs. T0 -25.9%, p=0.002, T2 vs. T0 -31.8%, p=0.005) systolic blood pressure (T1 vs. T0 -6.7%, p=0.03; T2 vs. T0 -10.2% p=0.02) and BMI (T1 vs. T0 -3.3%, p=0.001; T2 vs. T0 -3%, p=0.02). Significant improvements from baseline of E/A ratio (T1 vs. T0 +15%, p=0.03; T2 vs. T0 +27.5%, p=0.003) and brachial FMD (T1 vs. T0 +50.7%, p=0.02; T2 vs. T0 +39.4%, p=0.04) were also seen. No significant changes in eGFR, lipids and arterial stiffness measures were seen. Conclusions: Intensification of treatment with DAPA 10 mg was accompanied by significant improvements in LVDF and endothelial-dependent vasodilation measures, which persist after 52 weeks of treatment. These preliminary observational results shed light on potential mechanisms responsible for cardiovascular protection with SGLT2i in T2D patients, even in absence of overt cardiovascular disease. Disclosure I. D9ippolito: None. E. De Carli: None. A. Andreadi: None. M. Romano: None. A. Galli: None. A. Capria: None. M. Massaro: None. P. Sbraccia: None. D. Della-Morte: None. A. Bellia: None. D. Lauro: None. Funding University of Rome
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