Have you noticed that your patients are being prescribed SGLT-2 inhibitors, even if they don’t have diabetes? If your patient asked, would you be able to explain why they are taking an SGLT-2 inhibitor?
Listen in to learn about how this new and fascinating class of medication that was designed for diabetes is now being prescribed for heart failure, too.
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SGLT-2 inhibitors are now a part of the American Heart Association’s updated heart failure guidelines. SGLT-2 inhibitors are now recommended, with or without T2D, and with HFpEF and HFrEF.
Four (of many) proposed theories for why SGLT-2 inhibitors improve heart failure outcomes:
- SGLT-2 inhibitors provide mild, but optimized diuretic effects. The beauty of the mild diuresis provided by SGLT-2 inhibitors that is unique among diuretics is that intravascular volume is spared. SGLT-2 inhibitors instead selectively target the interstitial fluid. This situation of lower interstitial volume with preserved intravascular volume, is an ideal because it promotes organ perfusion. (Tsampasiuan et al, 2021)
- SGLT-2 inhibitors decrease inflammation. SGLT-2 inhibitors have been shown to reduce inflammation when given as a diabetic agent. This reduction in inflammation has the potential to decrease processes related to inflammation, such as extracellular matrix breakdown and fibrosis. (Lopaschuk & Verma, 2020)
- SGLT-2 inhibitors increase cardiac energy efficiency. Ketones produce more ATP than glucose and free fatty for failing hearts. SGLT-2 inhibitors decrease ketone excretion into the urine, and thus provide better, more efficient energy source for the heart. (Selvaraj et al, 2020)
- SGLT-2 inhibitors decrease cardiac afterload. SGLT-2 inhibitors decrease endothelial cell activation, which directly results in vasorelaxation, a decrease in arterial wall stiffness, and less overall vascular resistance. (Lopaschuk & Verma, 2020)