Heart failure is not only due to low ejection fraction. Some hearts fail with reduced ejection fraction (HFrEF), and some hearts fail with preserved ejection fraction (HFpEF). And HFpEF is more a heterogeneous clinical syndrome than a singular disease.

Experts will clarify HFpEF phenotypes, identify HFpEF mimics, explore an evidence-based diagnostic approach, and identify the need for further testing during the case-based session,Preserved But Failing: Emerging Perspectives on Heart Failure With Preserved Ejection Fraction, Wednesday, October 9, at 9:15 am ET, in Room 206AB of the Boston Convention & Exhibition Center.

“HFpEF is characterized by myocardial dysfunction that results in disproportionate increases in left filling pressures to maintain cardiac output, resulting in pulmonary edema,” said Session Chair, Veronica Franco, MD, MSPH, FACC, Director of Pulmonary Vascular Disease Research Studies and Professor of Cardiovascular Disease at The Ohio State University.

Presenters will explore three primary HFpEF phenotypes during the session, in addition to several that are less common.

• Younger age, higher prevalence of smoking with preserved function, and left ventricular (LV) hypertrophy
• Older individuals with atrial fibrillation and left atrial enlargement
• Individuals with obesity who have diabetes, chronic kidney disease, concentric LV hypertrophy, and high renin

Identifying the appropriate therapies for HFpEF can be challenging given the heterogeneous nature of HF with multiple comorbidities and etiologies, Dr. Franco said. Sodium-glucose cotransporter-2 (SGLT2) inhibition and diuretics remain the basic therapeutic approaches, but it is important to identify the HFpEF phenotype to better tailor therapy to specific patient needs.

Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) plus other medications may be appropriate for those living with diabetes, while GLP-1 RAs alone may be helpful for those with obesity. Multiple hypertension and other medications may be important for those with arterial hypertension and/or ischemic heart disease, while patients with atrial fibrillation, iron deficiency, COPD, and other conditions need different approaches.

It is just as important to distinguish between HFpEF and its many mimics that can contribute to volume overload. Multiple cardiac causes, chest radiation therapy, iron overload, kidney and liver disease, and chronic venous insufficiency, among other conditions, can also mimic HFpEF.

“It is important to identify the distinct etiology, as there are specific medications and surgical treatments for these conditions,” Dr. Franco said. “Imaging studies, particularly cardiac magnetic resonance, are often very useful for diagnosis. A particularly important and underrecognized cause of restrictive cardiomyopathy, cardiac amyloidosis, can be identified with a technetium pyrophosphate scintigraphy nuclear scan.”

While there are now class 1 treatment recommendations for HFpEF, as well as many medications for underlying etiologies and comorbidities, there are still no FDA-approved therapies for pulmonary hypertension associated with HFpEF. Pulmonary arterial hypertension vasodilators are contraindicated in HFpEF, which complicates management of underlying comorbidities.

“Finding appropriate therapies for HFpEF is challenging given it represents a highly heterogeneous clinical syndrome with multiple different comorbidities and etiologies,” Dr. Franco said. “SGLT2 inhibitors and diuretics have changed clinical practice, but challenges remain.”