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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.
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.
Abstract:
Alterations of endothelial function, inflammatory activation, and nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway are involved in the pathophysiology of heart failure. Metabolic alterations have been studied in the myocardium of heart failure (HF) patients; alterations in ketone body and amino acid/protein metabolism have been described in patients affected by HF, as well as mitochondrial dysfunction and other modified metabolic signaling. However, their possible contributions toward cardiac function impairment in HF patients are not completely known. Recently, sodium-glucose co-transporter 2 inhibitors (SGLT2i) and glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) have emerged as a new class of drugs designed to treat patients with type 2 diabetes (T2D), but have also been shown to be protective against HF-related events and CV mortality. To date, the protective cardiovascular effects of these drugs in patients with and without T2D are not completely understood and several mechanisms have been proposed. In this review, we discuss on vascular and metabolic effects of SGLT2i and GLP-1 in HF patients.
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