The effect of sodium-glucose cotransporter 2 inhibitors on left cardiac remodelling in heart failure with reduced ejection fraction: Systematic review and meta-analysis.
Eur J Heart Fail
; 26(2): 373-382, 2024 Feb.
Article
em En
| MEDLINE
| ID: mdl-38235936
ABSTRACT
AIMS:
The therapeutic mechanism of sodium-glucose cotransporter 2 inhibitors (SGLT2i) on left cardiac remodelling in patients with heart failure with reduced ejection fraction (HFrEF) is not well-established. This study meta-analysed the impact of SGLT2i on left cardiac structure and function in patients with HFrEF. METHODS ANDRESULTS:
Online databases were queried up to April 2023 for trials reporting indicators of left cardiac structure and function in patients with HFrEF treated with SGLT2i. Data from studies were pooled using a random-effects model to derive weighted mean differences (WMDs) and 95% confidence intervals (CIs). Six trials were included (n = 555). Compared with control, SGLT2i significantly improved left ventricular end-diastolic volume (LVEDV; WMD -17.07 ml [-23.84, -10.31]; p < 0.001), LVEDV index (WMD -5.62 ml/m2 [-10.28, -0.97]; p = 0.02), left ventricular end-systolic volume (LVESV; WMD -15.63 ml [-26.15, -5.12]; p = 0.004), LVESV index (WMD -6.90 ml/m2 [-10.68, -3.11]; p = 0.001), left ventricular ejection fraction (WMD 2.71% [0.70, 4.72]; p = 0.008), and left atrial volume index (WMD -2.19 ml/m2 [-4.26, -0.11]; p = 0.04) in patients with HFrEF. SGLT2i use was associated with a non-significant trend towards a reduction in left ventricular mass index (WMD -6.25 g/m2 [-12.79, 0.28]; p = 0.06). No significant impact on left ventricular global longitudinal strain was noted (WMD 0.21% [-0.25, 0.67]; p = 0.38).CONCLUSIONS:
Sodium-glucose cotransporter 2 inhibitors improve cardiac structure and function in patients with HFrEF.Palavras-chave
Texto completo:
1
Base de dados:
MEDLINE
Assunto principal:
Disfunção Ventricular Esquerda
/
Insuficiência Cardíaca
Tipo de estudo:
Systematic_reviews
Limite:
Humans
Idioma:
En
Ano de publicação:
2024
Tipo de documento:
Article