Effect of sodium-glucose cotransporter 2 inhibitors on left atrial remodeling and prognosis in patients with type 2 diabetes and heart failure with reduced ejection fraction

Aims Sodium-glucose cotransporter 2 inhibitors (SGLT2is) have been found to minimize hospitalization for heart failure and cardiovascular death. Cardiac reverse remodeling may be a mechanism responsible for the favorable clinical efficacy of SGLT2is on heart failure. To date, few studies have examined their effects on the left atrium. Therefore, the purpose of this study was to explore whether SGLT2is improve left atrial adverse remodeling in patients with type 2 diabetes and heart failure with reduced ejection fraction (HFrEF).Methods A single-center, retrospective, observational study was conducted. Consecutive patients with type 2 diabetes and HFrEF hospitalized at the First Affiliated Hospital of Dalian Medical University for acute decompensated heart failure between 1 January 2019 and 1 March 2022 were identified. On the basis of their treatment strategies, the enrolled participants were classified into SGLT2i and non-SGLT2i groups. The primary end point was all-cause mortality. Changes in left atrial echocardiographic indices from baseline to follow-up were also assessed.Results A total of 198 patients (mean age: 63.96 +/- 12.11 years, 20.71% women) were included. Greater reductions from baseline were seen with SGLT2i in the left atrial diameter (P < 0.001), left atrial superior-inferior diameter (P = 0.027), left atrial transverse diameter (P = 0.020), left atrial volume (P = 0.005), and left atrial volume index (P = 0.004). Moreover, 48 cases (48.48%) in the SGLT2i group and 33 (33.33%) in the non-SGLT2i group showed left atrial reverse remodeling (P = 0.003). Survival analysis demonstrated significantly lower overall mortality in the SGLT2i group compared with the non-SGLT2i group.Conclusion This study found that SGLT2i therapy promoted left atrial structure reverse remodeling. This beneficial effect may be a vital mechanism by which SGLT2i improved clinical outcomes in patients with HFrEF.