Early Initiation of SGLT2 Inhibitor is Important Irrespective of Ejection Fraction

Abstract

Introduction Sodium Glucose Cotransporter inhibitor (SGLTi) has revolutionized the medical management of heart failure in the last decade. This molecule was initially described as a glucose-lowering agent but now it has been recommended in patients with chronic heart failure irrespective of ejection fraction and diabetic status. SGLT2 inhibitor reduces preload by natriuresis and diuresis, reduces afterload, decreases pulmonary artery pressure, improves myocardial energetics, and decreases myocardial fibrosis. It also reduces NTpro BNP levels in heart failure patients, decreases serum uric acid, and promotes weight loss. It has also been proposed that this molecule has a favorable effect on vascular remodeling. SGLT-2i improves cardiac output and attenuates maladaptive cardiac remodeling, chronic inflammation, oxidative stress, and endothelial dysfunction (ED) by restoring the activity of nitric oxide (NO) within the vascular endothelium. As was foreseeable this molecule became one of the foundation pillars in the management of heart failure with reduced as well as preserved ejection fraction. SGLT2i also has a reno-protective effect, particularly in patients with heart failure and diabetes. Evidence with SGLT2 inhibitor in Heart failure with preserved ejection fraction (HFpEF) DELIVER TRIAL has evaluated the effect of dapagliflozin on total (first and recurrent) heart failure events in patients with heart failure having preserved ejection fraction (HFpEF) or mildly reduced ejection fraction (HFmrEF). A total of 6263 patients with LVEF of more than 40 %, NHYA Class II-IV, and high NT-pro BNP (>300pg/ml in sinus rhythm and > 600pg/ml in patients with atrial fibrillation) were included over the total study period of two years. Dapagliflozin 10 mg was compared to placebo. In patients with HFmrEF and HFpEF, dapagliflozin reduced the risk of total heart failure events and heart failurerelated hospital admissions. (1)