Background: Sodium-glucose co-transporter 2 (SGLT-2) inhibitor has overwhelming evidence to improve left ventricular performance and remodelling in patients across heart failure (HF) phenotypes. However, its effects on the right ventricle (RV) and pulmonary artery systolic pressure (PASP) remain unclear.
Objective: To assess the impact of SGLT-2 inhibitor on RV function and PASP
Study selection: Studies reporting RV and PASP indices following SGLT-2 inhibitor treatment among HF patients were included in the analysis.
Methods: Two investigators independently searched PubMed, Google Scholar, and the Cochrane Library for relevant articles. Relevant studies from January 2020 to January 2025 were searched. The quality of included studies was assessed using the Newcastle-Ottawa scale. Variables were pooled using a random or fixed effects model to estimate weighted mean differences with 95% confidence interval. Restricted Maximum Likelihood method (REML) was used to assess heterogeneity.
Results: A total of 12 studies comprising 603 HF patients were eligible for analysis. Significant improvements on right ventricular function and pulmonary artery pressure after SGLT-2 inhibitor treatment were observed, including tricuspid annular plane systolic excursion (TAPSE) (weighted mean difference, 1.0 mm; 95% CI, 0.62, 1.38 mm; P < 0.00001), pulmonary artery systolic pressure (PASP) (weighted mean difference, -1/96 mmHg; 95% CI, -4.24, 0.32 mmHg; p=0.01), right ventricular fractional area change (RFAC) (weighted mean difference, 4.06; 95% CI, -1.33, 9.45; p<0.002), and right ventricular systolic excursion velocity (RV ‘s’) (weighted mean difference, 1.67 cm/s; 95% CI, -0.4, 3.75 cm/s; p<0.02).
Quadratic regression model showed a non-linear association between TAPSE and left ventricular ejection fraction (R2 = 0.4005)
Conclusion: The findings of the study demonstrate that SGLT-2 inhibitor improves RV performance and PASP in patients with HF irrespective of ejection fraction. This benefit is not entirely driven by the improvement in left ventricular function.