Why am I giving an SGLT-2 inhibitor for heart failure?

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:

  1. 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)
  2. 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)
  3. 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)
  4. 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)