Dapagliflozin Improves Heart Structure in HFpEF Patients with Type 2 Diabetes:Study

A new study published in the European Journal of Medical Research revealed that dapagliflozin, a sodium-glucose co-transporter 2 (SGLT2) inhibitor, significantly reduces myocardial fibrosis and enhances cardiac structure, exercise capacity, and metabolic control in patients with heart failure with preserved ejection fraction (HFpEF) and type 2 diabetes (T2D).

Over half of all heart failure cases globally are heart failure with preserved ejection fraction, which poses a serious clinical issue. The paucity of evidence-based disease-modifying treatments for HFpEF, in contrast to HFrEF, contributes to high morbidity, frequent hospitalizations, and unfavourable long-term results.

Myocardial fibrosis, which causes increased ventricular stiffness, poor relaxation, and unfavourable cardiac remodelling, is one of the main pathophysiological factors in HFpEF. Because of persistent hyperglycemia, oxidative stress, systemic inflammation, and microvascular dysfunction, patients with type 2 diabetes mellitus (T2D) have a larger burden of myocardial fibrosis, which exacerbates HFpEF outcomes.

With clinical trials like EMPEROR-preserved and DELIVER proving their role in lowering heart failure hospitalizations and improving cardiovascular outcomes in HFpEF patients, SGLT2 inhibitors have transformed the treatment of heart failure by offering advantages beyond glycemic control. Thus, this study examined the antifibrotic effects of dapagliflozin in diabetic HFpEF patients.

A total of 100 patients with HFpEF and T2D were randomized (1:1) to receive either dapagliflozin 10 mg daily or a placebo for a duration of 12 months in this study. The baseline extracellular volume fraction (ECV) was used for stratification. At baseline, 6 months, and 12 months, cardiac MRI-derived ECV was used to measure myocardial fibrosis. Changes in the 6-min walk test (6MWT) distance, HbA1c, and left ventricular mass index (LVMI) were secondary objectives.

In comparison to a placebo (− 0.8% [95% CI − 1.3 to − 0.4]; p < 0.001), dapagliflozin significantly decreased myocardium fibrosis (mean ΔECV: − 3.5% [95% CI − 4.2 to − 2.8]). Further advantages included increased physical capacity (+45 m vs. +10 m in 6MWT; p = 0.01), better glycemic control (HbA1c: − 1.2% vs. − 0.4%; p = 0.01), and larger decreases in LVMI (− 8.2 g/m2 vs. − 2.1 g/m2; p = 0.002).

Overall, this study shows that in individuals with HFpEF and T2D, dapagliflozin improves heart shape, glycemic management, and functional ability while also dramatically reducing myocardial fibrosis. These findings support the use of SGLT2 inhibitors in phenotype-guided treatment plans for HFpEF and reaffirm their antifibrotic and cardiometabolic advantages.

Source:

Albulushi, A., Askari, K. M., Al-Abedi, A. M., Al-Kulaibi, M. A., Hasan, M. S., Hosseini, Z., Al-Rahman, M. T., Tanoh, D. B., Hasan, A. S., Al-Helli, Y., & Basouni, A. (2025). Impact of SGLT2 inhibitors on myocardial fibrosis in diabetic HFpEF: a longitudinal study. European Journal of Medical Research, 30(1), 592. https://doi.org/10.1186/s40001-025-02834-7