Why the study?
Moderate mitral regurgitation due to mitral valve prolapse frequently coexists with HFpEF and contributes to progressive symptoms and left atrial remodelling, but the incremental effect of adding SGLT2i and MRA therapy to standard treatment was unclear.
Does adding a sodium–glucose cotransporter 2 inhibitor and a mineralocorticoid receptor antagonist to standard heart failure therapy improve functional status (≥1 NYHA class improvement) in ambulatory patients with HFpEF and moderate degenerative mitral regurgitation?
Cohort (n=64)
Does adding a sodium–glucose cotransporter 2 inhibitor and a mineralocorticoid receptor antagonist to standard heart failure therapy improve functional status (≥1 NYHA class improvement) in ambulatory patients with HFpEF and moderate degenerative mitral regurgitation?
In ambulatory patients with HFpEF and moderate degenerative mitral regurgitation, adding SGLT2i and MRA to standard therapy was associated with significantly better NYHA functional class improvement, favorable left atrial remodeling, and reduced risk of symptom worsening over 24 months.
Background Moderate mitral regurgitation due to mitral valve prolapse frequently coexists with heart failure with preserved ejection fraction (HFpEF) and contributes to progressive symptoms and left atrial remodelling. The incremental effect of adding metabolic–neurohormonal therapy to standard treatment remains unclear. Purpose To evaluate whether the addition of a sodium–glucose cotransporter 2 inhibitor (SGLT2i) and mineralocorticoid receptor antagonist (MRA) to standard HF therapy improves functional status, cardiac structure, and symptom stability over 24 months. Methods We prospectively followed 64 ambulatory patients (age 41–74 years; 37 women, 27 men) with LVEF ≥50% and moderate degenerative mitral regurgitation. All received diuretic, beta-blocker and ACE inhibitor; 32 patients received additional SGLT2i + MRA (extended therapy group). Primary endpoint: improvement of ≥1 NYHA class at 24 months. Secondary endpoints: NT-proBNP change at 6 months, left atrial volume index, E/e′ ratio, and symptom worsening requiring diuretic escalation. Time-to-event analysis was performed using Kaplan–Meier curves; multivariable Cox regression adjusted for age, sex, baseline NT-proBNP and LA volume. Results At 6 months, NT-proBNP decreased by 29% in the extended therapy group vs 8% in standard therapy (p = 0.008). At 24 months, functional improvement occurred in 59% vs 34% (p = 0.04). LA volume index decreased −7.5 ± 4.3 mL/m² vs −1.9 ± 3.8 mL/m² (p = 0.009); E/e′ improved −2.4 ± 1.6 vs −0.8 ± 1.5 (p = 0.02). Symptom worsening requiring diuretic escalation occurred in 2 (6.2%) vs 6 patients (18.7%); Kaplan–Meier analysis demonstrated greater freedom from deterioration in the extended therapy group (log-rank p = 0.04). In multivariable Cox regression, extended therapy independently predicted reduced risk of symptom worsening (HR 0.31; 95% CI 0.08–0.92; p = 0.03). No patient required hospitalization or mitral intervention. Conclusion In ambulatory HFpEF patients with moderate mitral regurgitation due to prolapse, adding SGLT2i + MRA to standard therapy was associated with sustained symptomatic improvement, favourable atrial remodelling, and significantly greater freedom from clinical deterioration over 2 years. These findings support a phenotype-oriented therapeutic strategy in this underexplored population.Photo 1
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Dimitrova et al. (2026) conducted a cohort in Heart failure with preserved ejection fraction (HFpEF) with moderate degenerative mitral regurgitation due to mitral valve prolapse (n=64). Sodium–glucose cotransporter 2 inhibitor (SGLT2i) plus mineralocorticoid receptor antagonist (MRA) added to standard therapy vs. Standard HF therapy alone (diuretic, beta-blocker, and ACE inhibitor) was evaluated on Improvement of ≥1 NYHA class at 24 months (p=0.04).
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