THE EFFECT OF GLIFLOZINS ON CARDIAC REMODELING

Abstract

Gliflozins reduce the risk of developing heart failure (HF) in patients with diabetes mellitus, and they have been shown to improve the prognosis of patients with HF across all ranges of left ventricular ejection fraction (LVEF) by preventing HF decompensation and cardiovascular death [1]. In this connection, the question arises as to what other mechanisms underlie these effects besides the inhibition of the sodium-glucose cotransporter. The effect of gliflozin on cardiac remodeling, assessed by imaging and the related biomarkers, remains uncertain, while the number of studies involving patients with HF and the contradictory results have been focused mainly on patients with diabetes mellitus and reduced LVEF [2,3]. regardless of LVEF. Adverse myocardial remodeling affecting the left ventricle is a key factor in the progression of HF, and the current well-established HF phenotypes are based on LVEF. Nevertheless, other relevant players have received less attention, such as the left atrium. Indeed, the left atrium plays a decisive role in cardiac function, especially in the filling of the left ventricle (LV) during diastole. In addition, atrial dysfunction may directly lead to pulmonary congestion. Left atrial (LA) remodeling occurs in HF regardless of the degree of LV systolic dysfunction and may be observed with preserved or reduced LV [4,5]. Left atrial geometry is a predictor of the development of HF in high-risk patients [5] and is consistently associated with higher rates of hospitalization and mortality in patients with HF [6,7]. As a result, atrial disease has become an important concept that was highlighted in the most recent HF guidelines of the European Society of Cardiology (ESC) [8]. The aim of this study was to examine the effect of gliflozins on the parameters of cardiac remodeling, in particular LA remodeling, in patients with HF regardless of their LVEF.