Sodium-glucose cotransporter-2 inhibitors (SGLT2i) may revert the deleterious pathophysiologic interaction between diabetes mellitus and heart failure, leading to beneficial outcomes.
Do SGLT2 inhibitors improve outcomes in patients with coexisting diabetes mellitus and heart failure?
This review highlights the pathophysiologic interaction between diabetes and heart failure and the beneficial role of SGLT2 inhibitors in managing these coexisting conditions.
Diabetes mellitus (DM) and heart failure (HF) are frequently encountered afflictions that are linked by a common pathophysiologic background. According to landmark studies, those conditions frequently coexist, and this interaction represents a poor prognostic indicator. Based on mechanistic studies, HF can be propagated by multiple pathophysiologic pathways, such as inflammation, oxidative stress, endothelial dysfunction, fibrosis, cardiac autonomic neuropathy, and alterations in substrate utilization. In this regard, DM may augment myocardial inflammation, fibrosis, autonomic dysfunction, and lipotoxicity. As the interaction between DM and HF appears critical, the new cornerstone in DM and HF treatment, sodium-glucose cotransporter-2 inhibitors (SGLT2i), may be able to revert the pathophysiology of those conditions and lead to beneficial HF outcomes. In this review, we aim to highlight the deleterious pathophysiologic interaction between DM and HF, as well as demonstrate the beneficial role of SGLT2i in this field.
Theofilis et al. (Fri,) conducted a review in Diabetes mellitus and heart failure. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) was evaluated. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) may revert the deleterious pathophysiologic interaction between diabetes mellitus and heart failure, leading to beneficial outcomes.