Rethinking HFpEF Screening and Care, With Ronald D'Agostino, DO

The 2026 ACC Expert Consensus Decision Pathway repositions HFpEF management around a 2-drug backbone of SGLT2 inhibitors and nonsteroidal MRAs, diverging from the 4-pillar HFrEF regimen built on ACE inhibitors, ARBs, ARNIs, and beta-blockers.¹ Finerenone is now favored over spironolactone as the MRA of choice, and beta-blockers are reserved for atrial fibrillation, arrhythmia, or post-MI indications rather than routine use.¹ In patients with a BMI of 30 kg/m² or higher, the pathway recommends semaglutide or tirzepatide to address visceral adiposity, drawing on STEP-HFpEF and SUMMIT trial data.¹

The updated pathway also reframes HFpEF as a multisystem syndrome requiring coordinated management of obesity, sleep apnea, diabetes, and CKD rather than cardiology-only oversight.¹ Diuretics remain useful for volume overload but are directed toward as-needed rather than fixed daily dosing.¹ Early recognition remains a persistent barrier in office practice.

The H2FPEF score estimates the probability of HFpEF in symptomatic patients using 6 clinical and echocardiographic variables.² It gives office-based clinicians a structured tool to move past reflexive within-normal-limits readings and pursue BNP testing, echocardiography, or cardiopulmonary stress testing.² Five-year mortality for both HFrEF and HFpEF approaches 75% once patients reach the emergency department in decompensated heart failure, underscoring the value of earlier, stage A intervention.

These themes anchored “Getting to the Heart of the Matter: Recognition to Treatment Optimization of Heart Failure”, a clinical forum focused on cardiovascular risk factors, phenotype-guided staging, and evidence-based pathways to slow heart failure progression, moderated by Ronald D'Agostino, DO.

Following the forum, D'Agostino spoke with HCPLive to recap the discussion and expand on how the updated pathway changes daily practice. Below, he shares his perspective on phenotype-specific treatment and multidisciplinary comorbidity management.

Q&A: Treating HFpEF as Its Own Disease

HCPLive: What is the single biggest change in the updated heart failure guidelines clinicians need to know?

Ronald D'Agostino, DO: The recent HFpEF guidelines focus on SGLT2 inhibitors and nonsteroidal MRA as the backbone of treatment for HFpEF, which is different from the general heart failure guidelines, which have mostly focused on HFrEF and emphasized the 4 pillars of therapy: ACE inhibitor, ARB, or ARNI therapy, beta-blocker therapy, SGLT2 inhibitors, and MRA in general, emphasizing nonsteroidal agents. To me, that's a very big change: 2-pronged rather than 4-pronged, focusing on nonsteroidal MRA and SGLT2 rather than ACE inhibitor, ARB, or ARNI and beta-blocker, and even saying to probably avoid beta-blockers unless there is some compelling reason to use them, such as AFib or other arrhythmias that require beta-blocker therapy, or post-MI. The focus and emphasis are different because they represent different disease states, and the guidelines emphasize that in the management.

The other thing I think is very important with the new guidelines is the focus on comorbidities, especially obesity, using GLP-1 therapy, not just for the obesity per se or the diabetes or the sleep apnea, but also for the heart failure benefit if patients are treated with a GLP-1 therapy, or are obese, or diabetic, or have sleep apnea, or are on CPAP. It's a big change in how we approach HFpEF, definitely multifactorial. You often need a team approach, not just one doctor. You need obesity management, endocrinology. A lot of these patients have CKD, so you need to involve nephrology, nutritional guidance, and exercise. Really focusing on it takes a village. That, to me, is a big change from the traditional guidelines.

HCPLive: How can office-based clinicians use tools like the H2FPEF score to catch heart failure earlier?

Ronald D'Agostino, DO: I think that was a great addition to the guidelines. The H2FPEF score helps you think about it. When you think of a patient who is heavy, has hypertension, or is elderly, the point score is helpful. Many patients will fall into that moderate risk category, and many are high risk. It helps you think about the condition and look for it, and maybe draw a BNP or do an echo, rather than just describe their symptoms of dyspnea on exertion, fatigue, deconditioning, or obesity. It helps you think of HFpEF, address it, look for it, and then manage it.

I always tell my students, a very popular acronym is WNL. It's popular to say WNL, like when you read any EKG or lab report, you'll see WNL a lot, and it traditionally means within normal limits, whether it's blood work, an EKG, or any kind of testing. But what I tell my students, and they always answer that way because that's how they're trained, is that what it really means is we never looked. If you don't look, you don't find. I think the H2FPEF score helps you look, because it opens your eyes to the possibility a patient has HFpEF, and that maybe you should do a BNP, an echo, or a cardiopulmonary stress test to try to identify and treat it.

HCPLive: How central is a comorbidity-first approach to moving the needle on heart failure outcomes?

Ronald D'Agostino, DO: I think it's very important. It's a pyramid. By the time the patient gets to the top of the pyramid and ends up in the ER with heart failure, as I highlighted in the presentation, the morbidity and mortality are very high. Five-year mortality is around 75%, whether it's HFrEF or HFpEF, so if you wait for the patient to end up in the ER in pulmonary edema, the prognosis is very poor. We discussed that at the meeting. But if you could identify earlier, at the bottom of the pyramid, a Class A patient who doesn't really have heart failure but has risk factors for it, comorbidities like obesity, hypertension, sleep apnea, and diabetes, and then address and treat the foundation, the prognosis will be better.

HCPLive: What is one takeaway you want every clinician to change in their practice tomorrow?

Ronald D'Agostino, DO: Treating HFpEF differently than HFrEF. It's a different animal, and we shouldn't be using the traditional therapies unless they're needed for other comorbidities as the initial approach. So the main one would be: identify. If I had to say number one, look for HFpEF, and two, don't treat it like HFrEF. It's a different algorithm, focusing on SGLT2 inhibitors and nonsteroidal MRAs, and there's only one MRA available right now. That was the key takeaway. Use beta-blockers if needed for issues like post-MI or AFib. Use ACE inhibitors, ARBs, or ARNIs if patients are still having heart failure, are still hypertensive, or their BNP is still high, as add-on therapy. Use diuretics judiciously, like furosemide. Don't just put everyone on 40 mg of furosemide, but use it if needed for fluid overload or edema, maybe on an as-needed basis rather than daily. The takeaway is to treat it differently. The guidelines are different for both conditions. Don't just apply the reduced-EF data that we traditionally use for HFrEF to treat HFpEF or HFmrEF, the mildly reduced ejection fraction group, as well.

Editor's Note: This transcript has been edited for grammar and clarity using AI tools.

References

1. Kittleson MM, Panjrath GS, Bates K, et al. Management of heart failure with preserved ejection fraction: 2026 ACC expert consensus decision pathway: a report of the American College of Cardiology Solution Set Oversight Committee. J Am Coll Cardiol. Published online July 23, 2026. doi:10.1016/j.jacc.2026.06.018

2. Reddy YNV, Carter RE, Obokata M, Redfield MM, Borlaug BA. A simple, evidence-based approach to help guide diagnosis of heart failure with preserved ejection fraction. Circulation. 2018;138(9):861-870. doi:10.1161/CIRCULATIONAHA.118.030093