Long-term SGLT2 inhibitor therapy improves myocardial strain and diastolic function in HFpEF: a retrospective study linking functional recovery to reduced myocardial fibrosis - Summary - MDSpire
Advertisement
SGLT2 Inhibitor Therapy Enhances Myocardial Strain and Diastolic Function in Patients with HFpEF: A Retrospective Analysis Linking Functional Improvement to Decreased Myocardial Fibrosis
To evaluate the effects of long-term SGLT2i treatment (≥6 months) on left ventricular global longitudinal strain (GLS), diastolic function parameters, and serum fibrosis markers in patients with HFpEF, and to explore potential mechanisms.
Approach:
Study Design: Retrospective cohort study involving 185 patients with HFpEF, divided into SGLT2i group (n = 93) and control group (n = 92).
Data Collection: Demographic data, echocardiographic parameters, and serological indicators were collected at baseline and during follow-up (median 12 months).
Statistical Analysis: Independent sample t-tests, Mann–Whitney U tests, chi-square tests, Pearson correlation analysis, multivariate linear regression, and Kaplan–Meier method were used for analysis.
Key Findings:
GLS improved significantly in the SGLT2i group (ΔGLS: -2.49% ± 0.54% vs. -0.44% ± 0.52%, P < 0.001).
NT-proBNP decreased by 30.4% in the SGLT2i group vs. 9.7% in the control group (P < 0.001).
Heart failure rehospitalization rate was significantly lower in the SGLT2i group (24.7% vs. 55.4%, P < 0.001).
ΔGLS was significantly positively correlated with ΔPⅢNP (r = 0.554, P < 0.001).
SGLT2i treatment was identified as an independent predictor of GLS improvement (β= -2.05, P < 0.001).
Interpretation:
Long-term SGLT2i treatment significantly improves myocardial strain, diastolic function, and clinical outcomes in patients with HFpEF, closely related to the reduction of myocardial fibrosis markers.
Limitations:
Retrospective design may introduce bias.
Single-center study limits generalizability.
Follow-up duration may not capture long-term effects.
Conclusion:
SGLT2i therapy significantly improves myocardial strain and diastolic function in HFpEF patients, closely related to the reduction of myocardial fibrosis markers.