Episode 212: Managing HFpEF

Hyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. 

Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.

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Treatment of HFpEF

Arreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?

Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.

Jordan: And that’s worth repeating, because people still think of these as “diabetes drugs.” They’re not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.

Dr. Arreaza: They’re also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.

Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That’s excellent for a disease where we historically had almost nothing that worked.

Jordan: They’re also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.

Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what’s next?

Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.

Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.

Dr. Arreaza: Something to remember: HFpEF patients don’t tolerate congestion well, and being “a little wet” is not benign. Let’s move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?

Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.

Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it’s worth talking through how these drugs actually work in the kidney.

Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.

Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.

Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you