SGLT-2i therapy suppresses the progression of HFrEF and cardiogenic edema through multiple mechanisms, including natriuretic, osmotic, and anti-inflammatory effects in pre-clinical models.
Does SGLT-2i therapy suppress cardiogenic edema and improve cardiac function in pre-clinical models of HFrEF?
This review highlights the pre-clinical mechanisms by which SGLT-2 inhibitors suppress cardiogenic edema and slow HFrEF progression, supporting their translational importance.
In heart failure with reduced ejection fraction (HFrEF), cardiogenic edema develops from impaired cardiac function, pathological remodeling, chronic inflammation, endothelial dysfunction, neurohormonal activation, and altered nitric oxide-related pathways. Pre-clinical HFrEF studies have shown that treatment with sodium-glucose cotransporter-2 inhibitors (SGLT-2i) stimulates natriuretic and osmotic/diuretic effects, improves overall cardiac function, attenuates maladaptive cardiac remodeling, and reduces chronic inflammation, oxidative stress, and endothelial dysfunction. Here, we review the mechanisms and effects of SGLT-2i therapy on cardiogenic edema in various models of HFrEF. Overall, the data presented suggest a high translational importance of these studies, and pre-clinical studies show that SGLT-2i therapy has a marked effect on suppressing the progression of HFrEF through multiple mechanisms, including those that affect the development of cardiogenic edema.
Sullivan et al. (Fri,) conducted a review in Heart failure with reduced ejection fraction (HFrEF). Sodium-glucose cotransporter-2 inhibitors (SGLT-2i) was evaluated. SGLT-2i therapy suppresses the progression of HFrEF and cardiogenic edema through multiple mechanisms, including natriuretic, osmotic, and anti-inflammatory effects in pre-clinical models.