Sodium glucose cotransporter-2 inhibitor was associated with an improvement in left ventricular systolic function in patients with type 2 diabetes mellitus with impaired left ventricular systolic function.

Aims: Recent studies indicated that sodium glucose cotransporter-2 inhibitors (SGLT2i) reduced heart failure hospitalization in patients with type 2 diabetes mellitus (T2DM). However, whether SGTL2i can improve left ventricular (LV) systolic and diastolic function remained unclear. This study aimed to compare the change in echocardiographic parameters in T2DM patients receiving SGLT2i with a different baseline LV ejection fraction (LVEF). The change in echocardiographic parameters was also compared between T2DM patients treated with SGLT2i and those treated with dipeptidyl peptidase-4 inhibitor (DPP4i).

Methods And Results: This multicentre cohort study consecutively enrolled 665, 119, and 132 T2DM patients treated with SGLT2i with a preserved (≥50%), moderately reduced (40-50%), and reduced baseline LVEF (<40%), respectively, with paired baseline and post-treatment echocardiographic data available between 1 June 2016 and 31 May 2018. There were 212 patients treated with DPP4i with paired baseline and post-treatment echocardiographic data available at the same time. For those patients treated with DPP4i, 45 patients had impaired baseline LVEF of <50%. Echocardiographic parameters, including LVEF, LV end-diastolic volume, LV end-systolic volume (LVESV), and LV diastolic function, were analysed at baseline and after treatment. After a median SGLT2i treatment period of 230 days, patients with reduced LVEF were associated with an improvement in LVEF from 29.4 ± 7.4% to 42.2 ± 15.2% (P < 0.0001) and decrease in LVESV from 133.2 ± 49.2 to 117.4 ± 60.1 mL (P = 0.0002). Patients with moderately reduced LVEF were associated with an improvement in LVEF from 44.8 ± 2.9% to 49.7 ± 12.4% (P < 0.0001) and decrease in LVESV from 90.7 ± 31.1 to 80.0 ± 36.2 mL (P = 0.0017). Patients with preserved LVEF did not show an improvement in LVEF and LVESV after SGLT2i treatment. There were no significant changes of LV end-diastolic volume, LV diastolic function, and LV wall thickness in three study groups after SGLT2i treatment. In contrast, patients with impaired baseline LVEF (<50%) did not show any change in LVEF and LVESV after DPP4i treatment.

Conclusions: Sodium glucose cotransporter-2 inhibitor was associated with an improvement in LV systolic function in patients with T2DM with reduced and moderately reduced LVEF. In contrast, DPP4i treatment was not associated with any improvement in LVEF among patients with impaired LVEF.