Heart failure with preserved ejection fraction (HFpEF) has become the most common subtype of heart failure, accounting for more than half of all cases, and is expected to become even more prevalent in the coming years due to an aging population and rising rates of obesity and diabetes.

At a session during the 46th Congress of the Cardiology Society of the State of São Paulo (SOCESP 2026), held from June 4 to 6, experts reviewed key advances in the diagnosis and treatment of HFpEF — a condition that often presents with dyspnea and exercise intolerance despite a preserved ejection fraction.

According to Múcio Tavares de Oliveira Junior, MD, a cardiologist and professor at the University of São Paulo Medical School (FMUSP), although the diagnosis of HFpEF may seem complex, approximately 80% of cases can be identified through a combination of clinical evaluation, biomarkers, and echocardiography, without the need for invasive tests.

Among the most commonly used tools are the H₂FPEF and HFA-PEFF scores, developed to estimate the diagnostic probability of the disease. Both help identify patients with a high probability of HFpEF and those who fall into an intermediate category, requiring further investigation. “I tend to use the H₂FPEF score more as it relies more on clinical data. I’m not an echocardiographer, so it’s much easier for me to rely on clinical criteria,” commented the specialist.

Despite the importance of these scores, echocardiography remains one of the cornerstones of diagnostic evaluation. According to Viviane Tiemi Hotta, MD, PhD, a cardiologist at the Heart Institute (InCor), FMUSP, new echocardiographic parameters and the 2025 update to the guidelines of the American Society of Echocardiography have helped increase diagnostic accuracy and reduce the number of cases classified as indeterminate.

The specialist emphasized that the assessment of diastolic function depends on the integration of multiple echocardiographic parameters, including mitral valve Doppler, tissue Doppler imaging, systolic pulmonary artery pressure, and left atrial (LA) structural measurements. “Some authors often say that indexed LA volume is the ‘glycated hemoglobin of diastole,’” she stated, explaining that progressive chamber dilation reflects chronic exposure to elevated filling pressures.

In addition to traditional structural measurements, Hotta also emphasized LA strain, a parameter that assesses chamber deformation and can help identify earlier changes, even before structural dilation occurs. While LA volume reflects chronic exposure to elevated filling pressures, LA strain serves as a more sensitive marker of subclinical diastolic dysfunction.

When Rest Doesn’t Tell the Whole Story

Despite advances in diagnostic scores and echocardiographic assessment, some patients remain in a gray area. In these cases, tests performed at rest may not be sufficient to demonstrate the hemodynamic changes characteristic of the disease. “The problem is that the patient’s symptoms occur during exercise, but we assess them at rest,” summarized José Alexandre da Silveira, MD, a cardiologist and general coordinator of the ABCDM regional chapter of SOCESP.

To illustrate this scenario, the specialist presented the case of a 67-year-old female patient with progressive dyspnea for the past 18 months. Despite a preserved ejection fraction, only mildly elevated biomarkers, and an ECG without conclusive findings, the clinical suspicion of HFpEF remained high.

According to Silveira, patients with intermediate scores, borderline biomarkers, and inconclusive test results are those who benefit most from further investigation. In this situation, invasive hemodynamic assessment during exercise can reveal abnormalities that are not observed at rest. “The resting test is often misleading,” he stated.

In the case presented, filling pressures were normal at rest but increased significantly during exercise, confirming the diagnosis of occult exercise-induced heart failure. The specialist emphasized, however, that invasive exercise hemodynamics remains reserved for selected cases. “When we talk about invasive exercise hemodynamic testing, it is the gold standard. However, it is the exception,” he said. In his clinical practice, less than 5% of Silveira’s patients require this type of investigation.

According to him, the method’s greatest value lies in transforming diagnostic uncertainties into definitive diagnoses, allowing for the implementation of treatments capable of improving quality of life and functional capacity and reducing hospitalizations. “In the vast majority of cases, clinical presentation remains the guiding factor,” he concluded.

Treatment Begins With the Patient’s Phenotype

While the diagnosis of HFpEF remains a challenge, treatment has also undergone a significant transformation in recent years. According to Silas Ramos Furquim, MD, a cardiologist specializing in heart failure and transplantation at InCor/FMUSP, the syndrome is no longer viewed as a single disease but is now understood as a set of distinct phenotypes, each with different pathophysiologic mechanisms and therapeutic needs. “Treating only the ‘HFpEF’ label is a thing of the past,” he stated.

According to the cardiologist, obesity, diabetes, chronic kidney disease, atrial fibrillation, pulmonary hypertension, and cardiac amyloidosis now guide increasingly individualized therapeutic decisions, influencing both prognosis and treatment selection.

Among the most significant advances, the specialist highlighted SGLT2 inhibitors, which have established themselves as one of the main treatments for patients with HFpEF following the EMPEROR-Preserved and DELIVER studies. In addition, new evidence is expanding the role of medications targeted at specific disease phenotypes.

When discussing the cardiometabolic phenotype — characterized by obesity and systemic inflammation — Furquim emphasized that the treatment of obesity is now viewed not only as the management of a risk factor but also as part of the therapeutic strategy for HFpEF itself. The cardiologist cited recent studies with GLP-1 receptor agonists, such as the STEP-HFpEF trial, published in 2023 in The New England Journal of Medicine, which showed that semaglutide was able to improve symptoms, quality of life, and functional capacity in patients with obesity and HFpEF.

The speaker also highlighted the results of the SUMMIT study, published in 2024, in which tirzepatide reduced the risk for cardiovascular death or worsening heart failure by 38%. Finerenone, meanwhile, became part of the standard of care following the results of the FINEARTS-HF study, also published in The New England Journal of Medicine, which demonstrated a reduction in heart failure-related events in this population. “Treating heart failure based solely on its label is over. The future truly lies in precision medicine,” he concluded.

This story was translated from Medscape’s Portuguese edition.