Sodium-glucose co-transporter 2 inhibitors in left ventricular assist device and heart transplant recipients: a mini-review
- PMID: 39514145
- PMCID: PMC11802697
- DOI: 10.1007/s10741-024-10465-z
Sodium-glucose co-transporter 2 inhibitors in left ventricular assist device and heart transplant recipients: a mini-review
Abstract
In recent years, sodium-glucose co-transporter 2 inhibitors (SGLT2i) emerged as promising therapeutic agents in managing heart failure (HF). They demonstrated a significant impact on reducing HF hospitalizations and related mortality in patients with reduced and preserved ejection fraction. However, evidence supporting their use in patients with left ventricular assist device (LVAD) and heart transplant (HT) recipients is still limited. We identified six key studies investigating the safety and efficacy of SGLT2i in LVAD and HT recipients. In patients with LVAD, prescription of SGLT2i was predominantly associated with improved fluid management and reduced pulmonary artery pressures. However, the results regarding their effects on body weight, hemoglobin A1c, diuretic use, and right ventricular function were contradictory. In terms of safety, SGLT2i were generally well-tolerated in the LVAD population, and the reported incidence of adverse events was low. In HT recipients, SGLT2i were associated with better glycemic control and weight reduction. No relevant adverse events were reported. Despite these encouraging results, the long-term safety and efficacy of SGLT2i in these vulnerable patient populations are yet to be investigated. Future randomized controlled trials are needed to address existing gaps in evidence and help integrate SGLT2i into clinical practice for LVAD and HT recipients.
Keywords: Diabetes mellitus; Heart failure; Heart transplantation; Left ventricular assist device; Sodium-glucose co-transporter 2 inhibitor.
© 2024. The Author(s).
Conflict of interest statement
Declarations. Conflict of interest: E. A. reports educational and training grant from the European Society of Cardiology (ESC), congress grants from the Heart Failure Association of the ESC, congress grants from the German Society of Cardiology and German Society of Internal Medicine, all unrelated to this article. M.P.N. reports speaker fees by AstraZeneca and Vifor Pharma unrelated to the article, consultancy fees by Boehringer Ingelheim and Pierre Fabre, and congress travel support by Pfizer, all unrelated to the article. H.R. reports personal fees from Daiichi Sankyo, Pfizer, MedUpdate, StreamedUp, DiaPlan, NeoVasc, Pluristem, NovoNordisk and Corvia. institutional grants from Pluristem, BMS, Pfizer, Bard and Biotronik. A.J.F. reports fees from Alnylam, AstraZeneca, Bayer, Boehringer Ingelheim, Bristol Myers Squibb, Fresenius, Medtronic, MSD, Mundipharma, Novartis, NovoNordisk, Pierre Fabre, Pfizer, Roche, Vifor, and Zoll, as well as grant support by Novartis, AstraZeneca and Berlin Heart unrelated to this article. All other authors declare no conflict of interest.
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