# Efficacy of SGLT2 Inhibitors on Clinical Outcomes After Transcatheter Aortic Valve Replacement: A Systematic Review and Meta‐Analysis

**Authors:** Shaikh Muhammad Daniyal, Naveen Murad Khatoon, Anas Rasool, Isbah Gul, Sabula Tabish, Shireen Asifa, Ayan Khalid, Zunaira Aftab, Muhammad Burhan, Syeda Laiba Fahim, Habiba Tauqir Gondal, Muhammad Asfandyar Nadir, Syed Zaeem Ahmed, Danish Ali Ashraf, Somaiya Ahmed

PMC · DOI: 10.1002/edm2.70184 · 2026-02-26

## TL;DR

SGLT2 inhibitors may reduce mortality and heart failure hospitalizations after aortic valve replacement, but more research is needed.

## Contribution

This study is the first to evaluate the impact of SGLT2 inhibitors on outcomes after transcatheter aortic valve replacement.

## Key findings

- SGLT2 inhibitors reduced the composite outcome of mortality or heart failure hospitalization after TAVR.
- The drugs also lowered all-cause mortality and heart failure hospitalizations individually.
- Larger randomized trials are needed to confirm these findings.

## Abstract

Sodium‐glucose cotransporter 2 (SGLT2) inhibitors improve cardiovascular (CV) outcomes in patients with heart failure (HF) and type 2 diabetes. Their effect in patients undergoing transcatheter aortic valve replacement (TAVR) for severe aortic stenosis (AS), however, remains unclear. This study evaluated whether SGLT2 inhibitors reduce all‐cause mortality and HF hospitalisations after TAVR.

A systematic search of PubMed, ScienceDirect, Cochrane (CENTRAL), Scopus and Embase was performed through April 2025 for studies comparing post‐TAVR outcomes between SGLT2 inhibitor users and non‐users. Outcomes of interest included a composite of all‐cause mortality or heart failure (HF) hospitalisation, along with the individual components of all‐cause mortality and HF hospitalisation. All outcomes were extracted at 1 year. Pooled hazard ratios (HRs) with 95% confidence intervals (CIs) were calculated using a random‐effects model. Heterogeneity was quantified using I
2 statistics. Analyses were conducted in R (version 4.4.2).

Three studies (1 RCT, 2 Observational) comprising 3187 patients met inclusion criteria. SGLT2 inhibitor use was associated with a reduced risk of the composite outcome (HR: 0.75; 95% CI: 0.65, 0.86; p < 0.01). Individually, therapy lowered all‐cause mortality (HR: 0.72; 95% CI: 0.53, 0.96; p = 0.03) and HF hospitalisations (HR: 0.74; 95% CI: 0.61, 0.90; p < 0.01).

In patients with severe AS undergoing TAVR, SGLT2 inhibitors were associated with significant reductions in all‐cause mortality and HF hospitalisations. These findings suggest a promising role for SGLT2 inhibitors in improving post‐TAVR outcomes. However, given the limited data, larger randomised clinical trials are necessary to consolidate these findings.

Trial Registration: CRD420251132729

SGLT2 inhibitor therapy was associated with a significantly lower risk of the composite outcome of all‐cause mortality or heart failure hospitalization at one year, as well as each component individually.

## Linked entities

- **Diseases:** heart failure (MONDO:0005252), type 2 diabetes (MONDO:0005148)

## Full-text entities

- **Genes:** SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, AP2B1 (adaptor related protein complex 2 subunit beta 1) [NCBI Gene 163] {aka ADTB2, AP105B, AP2-BETA, CLAPB1}, NOS2 (nitric oxide synthase 2) [NCBI Gene 4843] {aka HEP-NOS, INOS, NOS, NOS2A}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}
- **Diseases:** atrial fibrillation (MESH:D001281), CKD (MESH:D012080), HFpEF (MESH:D054144), calcified (MESH:D018333), coronary artery disease (MESH:D003324), cardiac damage (MESH:D006331), cardiac remodelling (MESH:D020257), HF (MESH:D006333), renal dysfunction (MESH:D007674), type 2 diabetes (MESH:D003924), chronic kidney disease (MESH:D051436), valvular conditions (MESH:D006349), diabetes (MESH:D003920), malignancy (MESH:D009369), renal insufficiency (MESH:D051437), myocardial remodelling (MESH:D064752), fibrosis (MESH:D005355), myocardial disease (MESH:D004194), metabolic (MESH:D008659), acute kidney injury (MESH:D058186), COPD (MESH:D029424), AS (MESH:D001024)
- **Chemicals:** Dapagliflozin (MESH:C529054), Glucose Cotransporter (-), empagliflozin (MESH:C570240)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Figures

4 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12942055/full.md

---
Source: https://tomesphere.com/paper/PMC12942055