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SGLT2 inhibitors and left atrial function in heart failure with reduced or mildly reduced ejection fraction
Hakan Duman1, Hüseyin Durak2, Mustafa Çetin1
1Department of Cardiology, Faculty of Medicine, Recep Tayyip Erdoğan University, Rize, 53100, Türkiye.
Insights
Sodium-glucose cotransporter-2 (SGLT2) inhibitors did not improve left atrial (LA) function in heart failure (HF) patients with reduced ejection fraction (EF). LA structure and function were mainly influenced by diastolic dysfunction and ventricular remodeling, not SGLT2 therapy.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Sodium-glucose cotransporter-2 (SGLT2) inhibitors are established treatments for heart failure (HF), reducing mortality and hospitalizations.
- The impact of SGLT2 inhibitors on left atrial (LA) structure and function in HF patients with reduced or mildly reduced ejection fraction (EF) is not well understood.
Purpose of the Study:
- To investigate the effects of SGLT2 inhibitors on left atrial (LA) structure and function in patients with heart failure (HF) and reduced or mildly reduced ejection fraction (EF).
Main Methods:
- An observational, cross-sectional study involving 134 HF patients with EF < 50%, divided into SGLT2 inhibitor users (SGLT2+) and non-users (SGLT2-).
- Echocardiographic measurements included LA volume index (LAVI), LA emptying fraction (LAEF), and LA functional index (LAFI).
- Clinical, laboratory, and echocardiographic parameters were compared, and correlations with LA indices were analyzed using multivariable linear regression.
Main Results:
- The SGLT2+ group had higher prevalence of diabetes mellitus, spironolactone, and furosemide use.
- Lower left ventricular ejection fraction (LVEF) and larger left ventricular volumes were observed in the SGLT2+ group.
- A significant reduction in LA functional index (LAFI) was found in the SGLT2+ group, but no significant differences in LAVI or LAEF were observed between groups.
Conclusions:
- SGLT2 inhibitor use was not associated with improved LA volume or functional parameters in HF patients with reduced or mildly reduced EF.
- LA function's prognostic value is primarily linked to diastolic dysfunction and ventricular remodeling, rather than SGLT2 inhibitor therapy.
Background:
Sodium-glucose cotransporter-2 (SGLT2) inhibitors reduce cardiovascular mortality and hospitalizations in heart failure (HF). However, their effects on left atrial (LA) structure and function remain unclear, particularly in patients with reduced or mildly reduced ejection fraction (EF).
Methods:
This observational, cross-sectional study included 134 patients with HF and EF < 50%, divided into two groups: those receiving SGLT2 inhibitors (SGLT2+, n = 25) and those not receiving them (SGLT2-, n = 109). Echocardiographic measurements of LA volume index (LAVI), LA emptying fraction (LAEF), LA functional index (LAFI), and passive/active emptying fractions were obtained according to ASE/EACVI guidelines. Clinical, laboratory, and echocardiographic parameters were compared between groups, and correlations with LA indices were analyzed using multivariable linear regression.
Results:
The prevalence of diabetes mellitus, spironolactone use, and furosemide use was significantly higher in the SGLT2 + group (all p < 0.05). LVEF was lower (32.9 ± 6.7 vs. 38.7 ± 8.6, p = 0.002), and left ventricular volumes were larger in the SGLT2 + group, while LAFI was significantly reduced (0.12 ± 0.08 vs. 0.18 ± 0.10, p = 0.008). However, there were no significant differences in LAVI or LAEF between groups. Multivariable regression identified E/A ratio, age, and LVEF as independent determinants of LAVI; posterior wall thickness and E/A ratio for LAEF; and E/A ratio, diabetes mellitus, posterior wall thickness, and interventricular septal thickness for LAFI.
Conclusion:
SGLT2 inhibitor use was not associated with significant improvement in LA volume or functional parameters in patients with HF and reduced or mildly reduced EF. The prognostic value of LA functions appears to be primarily influenced by diastolic dysfunction and ventricular remodeling rather than SGLT2 inhibitor therapy.
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