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Sodium‐Glucose Cotransporter‐2 Inhibitors After Acute Myocardial Infarction: A Systematic Review and Meta-Analysis of Randomized Controlled Trials

  • Norman H Y Lin,
  • Jamie S. Y. Ho,
  • Aloysius S. T. Leow,
  • Yao Hao Teo,
  • Brian S. Y. Yeo,
  • Audrey A. Y. Zhang,
  • Fang Qin Goh,
  • Tiong-Cheng Yeo,
  • Raymond C. C. Wong,
  • Ping Chai,
  • Mark Y. Y. Chan,
  • Ching-Hui Sia

摘要

Background

Cardiovascular disease is on the rise globally, with ischemic heart disease being the leading cause of mortality and morbidity. While sodium-glucose cotransporter 2 inhibitors (SGLT2i) have been shown to improve cardiovascular outcomes in patients with heart failure, evidence is limited in guiding initiation in post-acute myocardial infarction (post-AMI) patients. Hence, this study aimed to appraise the current literature on the effect of SGLT2i on the clinical outcomes of post-AMI patients.

Methods

A comprehensive search of PubMed, EMBASE, SCOPUS, and ClinicalTrials.gov was conducted up to 1 May 2024. Only randomized controlled trials studying the use of SGLT2i in post-AMI patients were included. We included adult patients aged 18 years old and older diagnosed with AMI and initiated on SGLT2i in the acute post-AMI setting. SGLT2i studies solely in heart failure settings were excluded.

Results

Eight clinical trials were included in the systematic review, comprising 11,436 patients. Compared with placebo, SGLT2i initiation in post-AMI patients significantly reduced total number of heart failure hospitalizations (risk ratio [RR] 0.74, 95% confidence interval [CI] 0.62–0.90) and was associated with a lower N-terminal pro-B-type natriuretic peptide (NT-proBNP) level (− 26.67 pg/ml, 95% CI − 41.74 to − 11.59). There was no difference in all-cause mortality (RR 1.02, 95% CI 0.81–1.28), cardiovascular mortality (RR 1.03, 95% CI 0.83–1.28), change in left ventricular ejection fraction, and glycated hemoglobin (HbA1c), as compared with placebo.

Conclusion

SGLT2i use in patients with AMI was associated with a reduction in heart failure hospitalizations and a decrease in NT-proBNP. There were no significant differences in mortality outcomes.

Registration

PROSPERO identifier number CRD42024540843.

Graphical abstract