# Favorable association between early initiation of sodium-glucose cotransporter-2 inhibitors and in-hospital prognosis in acute myocardial infarction

**Authors:** Hung Thanh Quach, Anh Thi Kim Nguyen, Bao Quoc Dinh, Tuan Minh Nguyen, Hoang Huy Bui, Tuan Ngoc Tran, Tien Dung Ho, An Le Pham, Si Van Nguyen, Satoshi Higuchi, Satoshi Higuchi, Satoshi Higuchi, Satoshi Higuchi

PMC · DOI: 10.1371/journal.pone.0345315 · PLOS One · 2026-03-27

## TL;DR

Starting sodium-glucose cotransporter-2 inhibitors early in heart attack patients may improve survival during hospitalization.

## Contribution

This study is the first to show that early use of SGLT2i is independently linked to lower in-hospital mortality in acute myocardial infarction patients.

## Key findings

- Early initiation of SGLT2i within 24 hours of admission was associated with lower in-hospital mortality.
- Lower left ventricular ejection fraction and sepsis were independently linked to higher mortality.
- Use of BB/ACEi/ARB/MRA and early SGLT2i initiation were both independently associated with reduced mortality.

## Abstract

Acute myocardial infarction remains a major cause of death and disability worldwide, especially in low- and middle-income countries. Standard early management includes dual antiplatelet therapy, statins, beta-blockers (BB) and renin–angiotensin–aldosterone inhibitors (ACEi/ARB/MRA). Sodium–glucose cotransporter-2 inhibitors (SGLT2i) have been associated with favorable changes in cardiac function in acute myocardial infarction, but their impact on in-hospital mortality has not been well established.

To assess the association between early initiation of SGLT2i and in-hospital mortality among patients with acute myocardial infarction.

A retrospective, single-center study was conducted on 394 adult patients hospitalized with acute myocardial infarction at Nguyen Trai Hospital, Ho Chi Minh City, between January 2022 and October 2024. The data extraction and analysis were performed from July 31 to October 24, 2024. Patients with incomplete data, secondary acute myocardial infarction, or eGFR < 20 mL/min/1.73 m2 were excluded. Data from electronic medical records were analyzed. The primary outcome was in-hospital mortality. Logistic regression was used to identify independent predictors.

Mean age was 66.0 ± 11.7 years; 57.1% were male. SGLT2i was initiated within 24 hours of admission in 23.9% of patients. In-hospital mortality occurred in 53 patients (13.5%). In multivariable analysis, lower left ventricular ejection fraction (OR 0.91, 95% CI: 0.85–0.97; p = 0.003) and sepsis (OR 5.14, 95% CI: 1.04–25.36; p = 0.04) were independently associated with in-hospital mortality. In addition, use of BB/ACEi/ARB/MRA and early SGLT2i initiation were independently associated with lower in-hospital mortality (OR 0.12, 95% CI: 0.05–0.25; p < 0.001 and OR 0.27, 95% CI: 0.07–0.96; p = 0.04, respectively).

Together with traditional medical treatment, initiating SGLT2i within 24 hours of admission for acute myocardial infarction was independently associated with lower in-hospital mortality. These findings suggest a potential association between early SGLT2i use and improved in-hospital outcomes and warrant further investigation in prospective randomized studies.

## Linked entities

- **Diseases:** acute myocardial infarction (MONDO:0004781)

## Full-text entities

- **Genes:** MTOR (mechanistic target of rapamycin kinase) [NCBI Gene 2475] {aka FRAP, FRAP1, FRAP2, RAFT1, RAPT1, SKS}, SIRT1 (sirtuin 1) [NCBI Gene 23411] {aka SIR2, SIR2L1, SIR2alpha}, SLC5A2 (solute carrier family 5 member 2) [NCBI Gene 6524] {aka SGLT2}, PRKAA1 (protein kinase AMP-activated catalytic subunit alpha 1) [NCBI Gene 5562] {aka AMPK, AMPK alpha 1, AMPKa1}, AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, REN (renin) [NCBI Gene 5972] {aka ADTKD4, HNFJ2, RTD}
- **Diseases:** AMI (MESH:D009203), CKD (MESH:D012080), ischemic (MESH:D002545), acute kidney injury (MESH:D058186), shock (MESH:D012769), sepsis (MESH:D018805), Heart failure (MESH:D006333), chronic kidney disease (MESH:D051436), LV dilatation (MESH:D018487), inflammation (MESH:D007249), diabetes complications (MESH:D048909), macrovascular disease (MESH:D004194), infarct (MESH:D007238), type 2 MI (MESH:D003924), death (MESH:D003643), nephropathy (MESH:D007674), acute MI (MESH:D000208), neuropathy (MESH:D009422), MYOCARDIAL (MESH:D009202), retinopathy (MESH:D058437), diabetes (MESH:D003920), STEMI (MESH:D000072657)
- **Chemicals:** creatinine (MESH:D003404), DAPA (MESH:C020269), aldosterone (MESH:D000450), ATP (MESH:D000255), glucose (MESH:D005947), MRA (MESH:C502936), ACEi (-), fatty acid (MESH:D005227), heparin (MESH:D006493), ketone bodies (MESH:D007657), ketone (MESH:D007659), empagliflozin (MESH:C570240)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

14 references — full list in the complete paper: https://tomesphere.com/paper/PMC13028360/full.md

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Source: https://tomesphere.com/paper/PMC13028360