Background: Cardiac remodeling is defined as a group of molecular, cellular and interstitial changes that manifest clinically as changes in size, mass, geometry and function of the heart after injury. The process results in poor prognosis because of its association with ventricular dysfunction and malignant arrhythmias After MI, may predispose to ventricular rupture and aneurysm formation. Despite therapeutic advances, mortality rates related to cardiac remodeling/dysfunction remain HIGH. The term "remodeling" was used for the first time in 1982 by Hockman and Buckey, in a myocardial infarction (MI) model. This term was aimed to characterize the replacement of infarcted tissue with scar tissue. Postinfarct ventricular remodeling represents a prevailing cause of heart failure (HF), and it occurs in almost 30% of patients with a previous anterior myocardial infarction (MI) and in only approximately 17% of patients with non-anterior infarct. Adverse cardiac remodeling is an important contributor to heart failure severity. This includes the development of cardiac hypertrophy, fibrosis, inflammation, and cardiomyocyte cell death. Several experimental and human studies have demonstrated beneficial effects of SGLT2 inhibition on cardiac remodeling