Long-term SGLT2 inhibitor therapy improves myocardial strain and diastolic function in HFpEF: a retrospective study linking functional recovery to reduced myocardial fibrosis - Report - 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
SGLT2 Inhibitor Therapy Enhances Myocardial Strain and Diastolic Function
Overview
Long-term SGLT2 inhibitor treatment significantly improves myocardial strain and diastolic function in patients with HFpEF.
Background
Heart failure with preserved ejection fraction (HFpEF) is a complex syndrome that poses significant challenges in cardiovascular medicine. Myocardial fibrosis is a key feature of HFpEF, contributing to diastolic dysfunction and poor prognosis. Understanding the effects of SGLT2 inhibitors on myocardial function and fibrosis is crucial for improving patient outcomes.
Data Highlights
Parameter
SGLT2i Group
Control Group
P-value
ΔGLS
−2.49% ± 0.54%
−0.44% ± 0.52%
< 0.001
NT-proBNP Change
−30.4%
−9.7%
< 0.001
PⅢNP Change
−15.1%
−5.8%
< 0.001
GDF-15 Change
−20.5%
−8.6%
< 0.001
Rehospitalization Rate
24.7%
55.4%
< 0.001
Key Findings
Long-term SGLT2i treatment improved GLS significantly compared to controls.
NT-proBNP, PⅢNP, and GDF-15 levels decreased significantly in the SGLT2i group.
The rehospitalization rate for heart failure was significantly lower in the SGLT2i group.
ΔGLS was positively correlated with changes in fibrosis markers.
SGLT2i treatment was identified as an independent predictor of GLS improvement.
Clinical Implications
The findings suggest that SGLT2 inhibitors may provide significant benefits in managing HFpEF by improving myocardial strain and diastolic function. Monitoring fibrosis markers could be important in assessing treatment efficacy.
Conclusion
SGLT2 inhibitors demonstrate a beneficial impact on myocardial function and clinical outcomes in HFpEF patients.
Three of 23 patients experienced heart failure deterioration following medication withdrawal, while adverse drug events occurred only among patients who continued therapy.
