The Metabolic Model of Heart Failure; the Role of Sodium-Glucose Co-transporter 2(SGLT2) Inhibition

Abstract

The sodium-glucose co-transporter-2-inhibitors (SGLT2I) recently gained a unique role in managing the heart failure reduced ejection fraction. These inhibitors reduce cardiovascular (CV) risk factors, including plasma glucose, blood pressure, albuminuria, body weight, and renal events in the long term. The clinical trials proved their role in reducing hospitalization for HF, CV and all-cause mortality, atherosclerosis-related events, and CKD progression. Initiating this medication on decompensated heart failure or post-discharge reduces the risk of re-hospitalization. These co-transporter inhibitors reduced heart failure and kidney events regardless of baseline biomarker concentration or diabetes mellitus status. This article aims to the metabolic paradigm and cellular metabolism by exposing the available clinical trials of this novel therapy for heart failure, uncovering the possible mechanisms of action on the CV system, and describing the positive effect on prognostic markers as pro-BNP, as well as changing the plasma renin-aldosterone activity, cardiac troponin T (hs-cTnT), and insulin-like growth factor-binding protein 7 (IGFBP7).