Effect of Sodium Glucose Cotransporter 2 Inhibitiors on Left Ventricular Remodeling Among Diabetic and Non Diabetic Patients With Chronic Heart Failure

Sodium-glucose cotransporter 2 inhibitors (SGLT2i) have an established place in the therapy of heart failure (HF), as they have been shown to significantly reduce all-cause mortality, cardiovascular mortality, and hospitalizations in HFrEF patients, regardless of the presence of diabetes mellitus.

The growing evidence of the effect of SGLT2i on cardiac remodeling through cellular, molecular, vascular, interstitial, and electrical effects justifies its role as fundamental HF therapy.

SGLT2 inhibition in heart failure promotes reverse cardiac remodeling and is associated with better clinical outcomes.

Adverse myocardial remodeling affecting the left ventricle is a key factor in HF progression, and current well-established HF phenotypes are based on LVEF. However, other relevant players, such as the left atrium, have received less attention. Indeed, the left atrium plays a critical role in cardiac function, particularly in left ventricular (LV) filling during diastole. Additionally, atrial dysfunction can directly lead to pulmonary congestion. Left atrial (LA) remodeling occurs in HF irrespective of the degree of LV systolic dysfunction and can be observed in the presence of preserved or reduced LVEF. SGLT2 inhibition has been associated with reduced left ventricular (LV) and left atrial volumes in HF; however, its relationship with contemporary echocardiographic parameters of global LV systolic function, including global longitudinal strain and myocardial work, has not been thoroughly investigated.

Measuring the effect of SGLT2i therapy on left ventricular systolic function (LV) has previously been assessed by changes in heart size volume and ejection fraction.