Summary: In a randomised trial in patients with type 2 diabetes and heart failure with preserved ejection fraction, 12 months of dapagliflozin reduced cardiac-MRI-measured myocardial fibrosis and left-ventricular mass and improved glycaemia and walking distance compared with placebo.
PICO Summary
| Element | Detail |
|---|---|
| Population | 100 patients with HFpEF and type 2 diabetes; multicentre, double-blind. |
| Intervention | Dapagliflozin 10 mg daily for 12 months (cardiac MRI at baseline, 6, and 12 months). |
| Comparison | Placebo. |
| Outcome | Greater reduction in myocardial fibrosis (Δ extracellular volume -3.5% vs -0.8%; p<0.001), left-ventricular mass index (-8.2 vs -2.1 g/m²; p=0.002), HbA1c (-1.2% vs -0.4%; p=0.01), and 6-minute walk distance (+45 vs +10 m; p=0.01). |
Dapagliflozin and myocardial fibrosis in diabetic HFpEF
RCT · type 2 diabetes + HFpEF · 12 months
Over 12 months, dapagliflozin produced a larger regression in myocardial fibrosis (extracellular volume) and left-ventricular mass than placebo in diabetic HFpEF, with better glycaemia and walking distance. A small single-centre mechanistic trial of a surrogate imaging endpoint.
Expert Commentary
This is a mechanistically interesting study that tries to explain, with imaging, why SGLT2 inhibitors help in HFpEF, a question the large outcome trials answered clinically but not biologically. Showing a measurable regression in extracellular volume, a validated cardiac-MRI marker of diffuse myocardial fibrosis, alongside reduced ventricular mass and better functional capacity, offers a plausible disease-modifying narrative: that dapagliflozin does not merely relieve congestion but remodels the myocardium. I find the direction convincing and consistent with the class’s established benefit. My caveats concern magnitude and certainty. A 3.5% absolute fall in ECV over a year is sizeable for this measure and, in a single 100-patient study, warrants replication before being taken as definitive, and surrogate imaging endpoints are not themselves clinical outcomes. Can I use this with my patients? Yes, as reinforcement rather than novelty. SGLT2 inhibitors are already guideline therapy in HFpEF regardless of diabetes, and this adds a tangible mechanistic story, fibrosis regression, that can help explain to a patient why the drug is worth taking. The hard outcome evidence, not this, remains the basis for prescribing.
References
Albulushi A, Askari KM, Al-Abedi AM, et al. Impact of SGLT2 inhibitors on myocardial fibrosis in diabetic HFpEF: a longitudinal study. Eur J Med Res. 2025;30(1):592. doi:10.1186/s40001-025-02834-7