Efficacy of SGLT2 Inhibitors in Heart Failure to Improve Ejection Fraction

Background: Heart failure with reduced ejection fraction is a major cause of morbidity, hospital admission, and cardiovascular mortality worldwide. Many patients end up with poor functional status despite the standard heart failure treatment, frequent hospital admissions and worsening heart function. In recent years, sodium-glucose cotransporter-2 inhibitors have emerged as valuable therapeutic tools in the treatment of heart failure due to their salutary effects on cardiac function, ventricular remodeling, and on outcomes of heart failure. Objective: To determine the efficacy of empagliflozin in patients with chronic heart failure with reduced ejection fraction in terms of improvement in left ventricular ejection fraction, reduction in left ventricular end-systolic measurement, hospitalization for heart failure, urgent heart failure visits, and cardiovascular death. Methods: The study was a prospective, randomized controlled trial conducted from March 22, 2025 to June 22, 2025 in the Department of Medicine Unit 2, Peoples Medical College Hospital, Nawabshah. Fifty-six patients with chronic heart failure with reduced ejection fraction were included, and split into two halves. All patients in Group E received empagliflozin in addition to their usual heart failure treatment; all patients in Group P received placebo with their usual treatment. Demographic, clinical, laboratory and echocardiographic data were collected at baseline. At baseline and at 3 months, left ventricular ejection fraction and left ventricular end-systolic size were measured. Other data were also recorded such as hospitalisation for heart failure, urgent visits and cardiovascular death. Data were analysed using SPSS with a p value of ≤0.05 regarded as statistically significant. Results: Baseline characteristics were comparable between both groups. After three months, the Empagliflozin group showed a significantly greater improvement in mean left ventricular ejection fraction compared with the placebo group. Mean LVEF increased from 32.46 ± 4.18% to 41.82 ± 5.21% in the Empagliflozin group, while it increased from 32.89 ± 4.31% to 36.18 ± 4.96% in the placebo group. The mean improvement in LVEF was significantly higher in the Empagliflozin group. Left ventricular end-systolic measurement also decreased more markedly in the Empagliflozin group. Hospitalization for heart failure was significantly lower among patients receiving empagliflozin compared with placebo. Conclusion: Empagliflozin was effective in improving left ventricular ejection fraction and reducing left ventricular end-systolic measurement among patients with heart failure with reduced ejection fraction. It was also associated with a lower rate of hospitalization for heart failure. These findings support the use of empagliflozin as an effective add-on therapy in patients with chronic HFrEF.