Early initiation of empagliflozin in acute decompensated HFrEF significantly improved endothelial function (p-interaction=0.04) and left ventricular systolic and diastolic function at 2 months.
RCT (n=34)
randomized
Does early initiation of empagliflozin improve ventricular systolic and diastolic parameters, endothelial function, and arterial stiffness in patients with acute decompensated HFrEF?
Early initiation of empagliflozin in acute decompensated HFrEF significantly improves left ventricular systolic and diastolic function, as well as endothelial function, over a 2-month period.
p-value: p=0.04
Abstract Background Heart failure with reduced ejection fraction (HFrEF) is associated with endothelial dysfunction, arterial stiffness, and impaired ventricular function, contributing to poor outcomes. Sodium-glucose cotransporter-2 inhibitors (SGLT2i), such as empagliflozin, have demonstrated cardioprotective effects beyond glucose control, including potential benefits on vascular and myocardial function. However, their short-term impact in acute decompensated HF remains insufficiently explored. Purpose This study aimed to evaluate the short-term effects of empagliflozin on endothelial function, arterial stiffness, and indices of systolic and diastolic left ventricular (LV) function in patients hospitalized with acute or de novo HFrEF, independent of diabetes status. Methods Thirty-four patients with acute or newly diagnosed HFrEF were prospectively enrolled and randomized to receive either standard guideline-directed medical therapy (GDMT) alone (n=14) or with empagliflozin 10 mg daily (n=20) initiated within 24–72 hours of admission. GDMT included ACE inhibitors/ARNI, beta-blockers, mineralocorticoid receptor antagonists, and diuretics. Echocardiographic measures (LV ejection fraction (LVEF), LV global longitudinal strain (LV-GLS), E/e’, left atrial (LA) strain), endothelial function (flow-mediated dilation (FMD)), and arterial stiffness parameters (pulse wave velocity (PWV), augmentation index (Aix)) were assessed at baseline, one month, and two months. Results Baseline clinical characteristics and imaging parameters were comparable between groups. After two months, the empagliflozin group exhibited significant improvements in LV systolic (LVEF, LV-GLS) and diastolic function (E/e’, LA strain) compared to controls (Figure 1). Endothelial function, measured by FMD, significantly improved in the empagliflozin group (p=0.02) but remained unchanged in the control group (p-interaction=0.04). Arterial stiffness parameters (PWV, Aix) showed no significant differences between groups. Significant correlations were observed between ΔFMD-ΔLVEF (R=0.40, p=0.04) and ΔPWV-ΔE/e’ (R=0.44, p=0.03) (Figure 2). Conclusion Early initiation of empagliflozin in acute decompensated HFrEF significantly improved both left ventricular systolic and diastolic function with parallel improvement in endothelial function. Importantly the association between endothelial function improvement and LV systolic function suggests a potential mechanistic link between vascular and myocardial benefits. These findings underscore empagliflozin’s therapeutic potential beyond glycemic control, reinforcing its role in cardiovascular protection through endothelial-ventricular interaction in acute heart failure.Figure 1 Figure 2
Anastasiou et al. (Sat,) conducted a rct in Acute decompensated HFrEF (n=34). Empagliflozin vs. Standard guideline-directed medical therapy (GDMT) alone was evaluated on Endothelial function (FMD), arterial stiffness, and indices of systolic and diastolic left ventricular function (p=0.04). Early initiation of empagliflozin in acute decompensated HFrEF significantly improved endothelial function (p-interaction=0.04) and left ventricular systolic and diastolic function at 2 months.