Vascular and metabolic effects of SGLT2i and GLP-1 in heart failure patients

Michele Correale1, Olga Lamacchia2, Michele Ciccarelli3

  • 1Cardiology Department, Ospedali Riuniti University Hospital, Foggia, Italy. michele.correale@libero.it.

Heart Failure Reviews
|August 11, 2021
PubMed

Insights

Sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) show cardiovascular benefits in heart failure (HF) patients. This review explores their vascular and metabolic effects in HF, offering insights into their protective mechanisms.

Area of Science:

  • Cardiology
  • Metabolic Disorders
  • Pharmacology

Background:

  • Heart failure (HF) involves endothelial dysfunction, inflammation, and altered nitric oxide-cyclic guanosine monophosphate (NO-cGMP) signaling.
  • Metabolic changes, including ketone body, amino acid/protein metabolism, and mitochondrial dysfunction, are observed in HF patients, but their role in cardiac impairment is unclear.

Purpose of the Study:

  • To review the vascular and metabolic effects of sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) in heart failure (HF) patients.
  • To elucidate the proposed mechanisms behind the cardiovascular protective effects of SGLT2i and GLP-1 RAs in patients with and without type 2 diabetes (T2D).

Main Methods:

  • Literature review focusing on studies investigating SGLT2i and GLP-1 RAs in the context of heart failure.
  • Analysis of existing research on the vascular and metabolic pathways affected by these drug classes.

Main Results:

  • SGLT2i and GLP-1 RAs, initially developed for type 2 diabetes (T2D), demonstrate significant protective effects against HF events and cardiovascular mortality.
  • Evidence suggests these drugs impact endothelial function, inflammation, and metabolic signaling, contributing to cardiovascular benefits.

Conclusions:

  • SGLT2i and GLP-1 RAs represent a promising therapeutic strategy for managing heart failure, irrespective of diabetes status.
  • Further research is needed to fully understand the complex vascular and metabolic mechanisms underlying their cardioprotective actions in HF.

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