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Published on: April 8, 2013
Switch to gliflozins and biventricular function improvement in patients with chronic heart failure and diabetes
Michele Correale1, Pietro Mazzeo2, Martino Fortunato2
1Ospedali Riuniti University Hospital, Foggia, Italy.
Background:
SGLT2 inhibitors have been shown to reduce hospitalisation in patients with chronic heart failure (CHF). The cardioprotective mechanisms of gliflozins however have not been fully elucidated. The aim of this study was therefore to evaluate the effect of SGLT2 inhibitors on right and left ventricular function in patients with diabetes and HF.
Methods:
Seventy-eight patients with diabetes and CHF were enroled in the study and followed up; 38 started treatment with SGLT2i, while the remaining 40 continued their previous antidiabetic therapy. All patients underwent conventional, TDI and strain echocardiography in an ambulatory setting, at the beginning and after 3 months of therapy with SGLT2i.
Results:
After 3 months of therapy with SGLT2i, echocardiographic parameters assessing both left and right ventricular dimensions and function were found as significantly improved in patients switching to SGLT2i than control group: LVEF (45 ± 9% vs. 40 ± 8%, p < 0.001), LVEDD (54 ± 6.5 vs. 56 ± 6.5 mm, p < 0.01), GLS (-13 ± 4% vs. -10 ± 3%, p < 0.001), TAPSE (21 ± 3 vs. 19 ± 3 mm, p < 0.001), RV S' (12.9 ± 2.5 vs 11.0 ± 1.9 cm/sec, p < 0.001) and PAsP (24 ± 8 vs. 31 ± 9 mmHg, p < 0.001). Also mitral (1.0 ± 0.5 vs. 1.3 ± 0.5, p < 0.01) and tricuspid regurgitation (1.0 ± 0.5 vs. 1.3 ± 0.5, p < 0.01) improved after SGLT2i therapy. Changes were not statistically significant in patients not treated with SGLT2i (p n.s. in all cases).
Conclusions:
In a real-world scenario, treatment with SGLT2i in patients with CHF and diabetes is associated with an improvement in both left and right ventricular function assessed at echocardiography. These data may explain potential anti-remodelling effects of gliflozins.
Insights
Sodium-glucose cotransporter 2 (SGLT2) inhibitors significantly improved heart function in patients with diabetes and chronic heart failure (CHF). This real-world study demonstrates enhanced left and right ventricular function after SGLT2 inhibitor therapy.
Area of Science:
- Cardiology
- Endocrinology
- Pharmacology
Background:
- Sodium-glucose cotransporter 2 (SGLT2) inhibitors are known to reduce hospitalizations in patients with chronic heart failure (CHF).
- The precise cardioprotective mechanisms of SGLT2 inhibitors, also known as gliflozins, remain incompletely understood.
- This study aimed to investigate the impact of SGLT2 inhibitors on right and left ventricular function in individuals with diabetes and heart failure.
Purpose of the Study:
- To evaluate the effects of SGLT2 inhibitors on cardiac function.
- To assess changes in both left and right ventricular function.
- To explore these effects in patients with co-existing diabetes and heart failure.
Main Methods:
- Seventy-eight patients with diabetes and CHF were enrolled.
- 38 patients initiated SGLT2 inhibitor treatment, while 40 continued their existing antidiabetic therapy.
- Echocardiography, including conventional, tissue Doppler imaging (TDI), and strain imaging, was performed at baseline and after 3 months.
Main Results:
- SGLT2 inhibitor therapy led to significant improvements in left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), and global longitudinal strain (GLS).
- Right ventricular function also showed significant improvements, indicated by enhanced TAPSE and RV S' values.
- Pulmonary artery systolic pressure (PAsP) and both mitral and tricuspid regurgitation were reduced, with no significant changes observed in the control group.
Conclusions:
- SGLT2 inhibitors are associated with improved left and right ventricular function in patients with CHF and diabetes in a real-world setting.
- These findings suggest potential anti-remodeling effects of gliflozins.
- Echocardiographic assessment supports the beneficial impact of SGLT2 inhibitors on cardiac structure and function.
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