# SGLT-2 inhibitors improve cardiac function in hypertrophic cardiomyopathy: a real-world propensity score-matched study

**Authors:** Cong Ding, Fangchao Lv, Lin Wang, Xiaohong Xu

PMC · DOI: 10.3389/fcvm.2026.1742682 · Frontiers in Cardiovascular Medicine · 2026-02-12

## TL;DR

SGLT-2 inhibitors improve heart function in hypertrophic cardiomyopathy patients without causing major side effects.

## Contribution

This real-world study demonstrates the potential therapeutic value of SGLT-2 inhibitors in HCM patients.

## Key findings

- SGLT-2 inhibitors significantly improved diastolic function and NYHA class in HCM patients.
- No significant increase in hypoglycemia or renal dysfunction was observed with SGLT-2 inhibitors.
- Multivariate analysis confirmed sustained improvements in key cardiac parameters.

## Abstract

Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy and diastolic dysfunction. While sodium-glucose cotransporter 2 inhibitors (SGLT-2i) have demonstrated efficacy in heart failure (HF), their role in HCM remains underexplored. This real-world study aimed to evaluate the clinical efficacy of SGLT-2i in HCM patients.

A retrospective analysis was conducted on HCM patients admitted between January 2021 and December 2024. After PSM, 94 patients initiating SGLT-2i were compared with 94 controls. Primary endpoints included changes (Δ) in echocardiographic parameters and NYHA class at 6-month follow-up. Secondary endpoint was readmission for HF by June 2025. At 6-month follow-up, patients treated with SGLT-2i showed significantly greater improvements in key parameters compared to controls: septal e′ (Δ 0.7 ± 1.3 vs. Δ 0.04 ± 1.6 cm/s, p = 0.002), E/e′ (Δ −5.1 ± 8.7 vs. Δ 0.4 ± 6.4, p < 0.001), and IVST (Δ −1.3 vs. Δ −0.2 mm, p = 0.005), alongside a greater reduction in NYHA class [−1 (−1 to −0.25) vs. −1 (−1 to 0), p = 0.031]. Multivariate analysis confirmed sustained differences in improvements of septal e′ (t = 2.26, p = 0.025), E/e′ (t = −3.75, p < 0.001) and NYHA class (p = 0.038). No significant difference was found in HF readmission (20 events in SGLT-2i group vs. 17 in control group; log-rank p = 0.73) after 16.3-month median follow-up. No hypoglycemic events occurred and there was no significant deterioration in renal function.

SGLT-2i administration was associated with improved left ventricular diastolic function and NYHA class in HCM patients without increasing risks of renal dysfunction or hypoglycemia, supporting its potential therapeutic value in this population.

## Linked entities

- **Diseases:** hypertrophic cardiomyopathy (MONDO:0005045), heart failure (MONDO:0005252)

## Full-text entities

- **Genes:** SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, PIM1 (Pim-1 proto-oncogene, serine/threonine kinase) [NCBI Gene 5292] {aka PIM}, NPPB (natriuretic peptide B) [NCBI Gene 4879] {aka BNP, Iso-ANP}, MRGPRD (MAS related GPR family member D) [NCBI Gene 116512] {aka MRGD, TGR7}
- **Diseases:** HCM (MESH:D002312), cardiac remodeling (MESH:D020257), cardiac or systemic diseases (MESH:D006331), diabetic ketoacidosis (MESH:D016883), CAD (MESH:D003324), ICDs (MESH:D057873), renal dysfunction (MESH:D007674), HF (MESH:D006333), cardiac abnormalities (MESH:D018376), ventricular fibrillation (MESH:D014693), ventricular tachycardia (MESH:D017180), impaired quality of life (MESH:D003643), hypertension (MESH:D006973), LV hypertrophy (MESH:D017379), microvascular dysfunction (MESH:D017566), urinary tract infection (MESH:D014552), diastolic impairment (MESH:D006337), hypoglycemia (MESH:D007003), myocardial infarction (MESH:D009203), ischemic stroke (MESH:D002544), AF (MESH:D001281), hypertrophy (MESH:D006984), IVST (MESH:C563239), cardiomyopathy (MESH:D009202), COPD (MESH:D029424), pneumonia (MESH:D011014), SCD (MESH:D016757), stroke (MESH:D020521), LV diastolic dysfunction (MESH:D018487), structural abnormality (MESH:C566527), Arrhythmia (MESH:D001145), obstruction (MESH:D000402), hypoglycemic (MESH:C000721848), arrhythmic (OMIM:212500), LVOTO (MESH:D000092242), hereditary cardiomyopathy (MESH:D009386), fracture (MESH:D050723), inflammatory (MESH:D007249), fibrosis (MESH:D005355), CKD (MESH:D051436), renal insufficiency (MESH:D051437), DM (MESH:D003920)
- **Chemicals:** DAPA (MESH:C020269), creatinine (MESH:D003404), glucose (MESH:D005947), calcium (MESH:D002118), ARNI (-), Mavacamten (MESH:C000605992), dapagliflozin (MESH:C529054), blood sugar (MESH:D001786), uric acid (MESH:D014527)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935945/full.md

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Source: https://tomesphere.com/paper/PMC12935945