Diabetes Mellitus and Heart Failure: Epidemiology, Pathophysiologic Mechanisms, and the Role of SGLT2 Inhibitors

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.

Automated summary

Diabetes mellitus (DM) and heart failure (HF) have a common pathophysiologic background. HF can be caused by various pathways, including inflammation, oxidative stress, endothelial dysfunction, fibrosis, autonomic neuropathy, and alterations in substrate utilization. DM may aggravate myocardial inflammation, fibrosis, autonomic dysfunction, and lipotoxicity. The interaction between DM and HF is critical, and the new treatment approach, SGLT2 inhibitors (SGLT2i), may have beneficial effects in reversing the pathophysiology of these conditions and improving HF outcomes.