Abstract / Summary
Abstract Background Sodium–glucose cotransporter-2 (SGLT-2) inhibitors provide cardiovascular and renal benefits in patients with type 2 diabetes mellitus (T2DM), but prospective real-world evidence regarding their effects on echocardiographic parameters, pulmonary hemodynamics, and inflammatory status remains limited. This study evaluated changes in metabolic, cardiorenal, and inflammatory parameters observed during SGLT-2 inhibitor therapy in patients with T2DM. Methods This prospective, uncontrolled single-center cohort study included 51 patients with T2DM who initiated empagliflozin (10 mg/day) or dapagliflozin (10 mg/day) and were followed for six months. Clinical, biochemical, renal, and echocardiographic parameters, including left ventricular ejection fraction (LVEF), tricuspid annular plane systolic excursion (TAPSE), pulmonary artery systolic pressure (PASP), and Doppler-derived indices, were assessed at baseline and at 6-month follow-up and compared using paired statistical tests. Results After six months, significant reductions were observed in body mass index, systolic blood pressure, heart rate, HbA1c, urinary albumin, urinary creatinine, albumin-to-creatinine ratio, inflammatory markers, and ferritin, along with improvement in lipid profile. LVEF remained stable and TAPSE was unchanged, whereas pulmonary and aortic velocity time integrals and mitral E-wave velocity increased significantly; PASP increased modestly but remained within the normal physiological range. Conclusions SGLT-2 inhibitor therapy was associated with favorable changes in metabolic control, renal biomarkers, lipid profile, and inflammatory status, without evidence of decline in left ventricular systolic function, and with favorable changes in selected echocardiographic parameters in patients with T2DM. Given the observational, uncontrolled design of this study, these findings should be regarded as hypothesis-generating rather than confirmatory; larger controlled studies are needed to confirm these associations and clarify the effects of SGLT-2 inhibitors on pulmonary hemodynamics.