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HFpEF Management: 5 Things to Know

4. Physicians need to be mindful to protect the right ventricle of patients with HFpEF.

Both pulmonary hypertension and RV dysfunction are highly prevalent in HFpEF. RV dysfunction probably results from a combination of impaired RV contractile function and elevated RV afterload. Longitudinal HFpEF studies have shown that RV structure and function worsen over time; this deterioration has been associated with atrial fibrillation, coronary artery disease, obesity, and increased left heart and pulmonary venous pressures.

As left heart filling pressures rise, the pulmonary vasculature becomes less compliant, increasing RV afterload. In addition, remodeling of the pulmonary vasculature, including intimal thickening in the veins and intimal and medial thickening in the arteries, may occur. Therefore, tailored diuretic therapy to normalize left heart filling pressures and prevent pulmonary congestion is a mainstay of treatment for patients with HFpEF. Discharge diuretics were recently associated with both a reduction in 30-day HF rehospitalizations and mortality in patients with HF, independent of ejection fraction. In the setting of diuretic resistance, transitioning patients from furosemide to a loop diuretic with more consistent bioavailability (eg, bumetanide, torsemide) may also be helpful. Although thiazide diuretics may be used on an as-needed basis to facilitate diuresis, their daily use in conjunction with a loop diuretic should be limited in the outpatient setting owing to the risk for kidney injury and electrolyte abnormalities. Finally, implantable pulmonary artery pressure monitoring devices may be particularly useful in the HFpEF population to maintain and achieve euvolemia, proving effective in guiding diuretic therapy in order to reduce hospitalizations.

Although physiologically tempting, pulmonary vasodilator therapy is currently contraindicated in this population and may only be given to patients in a clinical trial setting. Two such studies, one testing whether sildenafil improves outcomes in patients with persistent pulmonary hypertension and the other evaluating the effects of macitentan on pulmonary hypertension with LV dysfunction, have suggested worse outcomes with these therapies.

5. Patients with refractory HFpEF should consider enrolling in clinical trials.

The lack of effective medical therapies for HFpEF has led researchers to reassess clinical trial designs for HFpEF. In particular, the delineation of specific clinical (eg, HFpEF with right heart failure), hemodynamic (eg, marked rise in left-sided filling pressures with exertion), and genetic (eg, amyloid) phenotypes is now shaping trial enrollment in an attempt to better match drug and device mechanisms to pathophysiologic mechanisms. (HFpEF with concomitant right ventricular failure, HFpEF with predominant exercise intolerance, and HFpEF due to amyloidosis are just some examples of phenotypic variants.) One example includes interatrial shunt devices that produce left-to-right shunts, lowering left atrial pressures (particularly during exertion). Initial studies on such devices have enrolled carefully selected patients with HFpEF whose hemodynamic profiles favor left-to-right shunting. Early results from ongoing major outcome trials, such as REDUCE LAP-HF I, have shown promise.

Physicians caring for patients with refractory HFpEF are strongly encouraged to refer them to a specialized center participating in clinical trials. Such participation may benefit not only these patients but others like them who are seriously in need

Stress Associated With HFpEF but Not HFrEF?

Stress was linked to higher long-term risk related to heart failure with preserved ejection fraction (HFpEF), researchers found from the large REGARDS cohort.

People who reported feeling more stress had more incident HFpEF-related death and hospitalization over a median follow-up of 10.1 years compared with peers scoring zero on the Perceived Stress Scale (PSS) assessment:

  • PSS score 1-2: adjusted HR 1.37 (95% CI 1.00-1.89)
  • PSS 3-4: adjusted HR 1.42 (95% CI 1.04-1.95)
  • PSS ≥5: adjusted HR 1.41 (95% CI 1.04-1.92)

In contrast, stress had no discernable relationship with incident HFrEF events, reported Lauren Balkan, MD, of Weill Cornell Medical Center in New York City, during her presentation at a moderated poster session at this year’s virtual conference of the Heart Failure Society of America.

HFpEF is thought to be a progressive systemic disorder influenced by aging and key comorbidities, such as chronic kidney disease and obesity. It is possible that psychological stress is another one of those comorbid conditions, Balkan suggested.

“We already know that lifestyle factors, including emotional and psychological stress, contribute to heart failure via increased oxidative stress and activation of inflammatory and neurohormonal pathways,” Balkan said.

The study was based on the REGARDS cohort of more than 30,000 U.S. study participants, originally examined to evaluate geographic and racial disparities in stroke mortality.

The ongoing longitudinal study enrolled patients in 2003-2007. Participants underwent a baseline physical examination and reported detailed sociodemographic information, dietary patterns, and medication use. Subsequently, they were contacted by phone every 6 months for updates on hospitalizations and mortality.

Balkan’s group analyzed the 25,785 REGARDS patients (45% men, 40% Black, mean age 64 years) who were free of heart failure and had the four-item PSS completed at baseline.

This cohort was divided into quartiles by PSS score.

People in higher stress categories were more likely to be female, Black, and have income below $35,000 per year. They also exhibited more unhealthy behaviors (e.g., current smoking, alcohol use, and no exercise), and had a higher prevalence of comorbidities such as atrial fibrillation.

But interactions for age, sex, and income were not significant.

Limitations of the observational study include its reliance on self-reported measures and the assessment of stress at a single time point, Balkan acknowledged.

  • author['full_name']

    Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow


The REGARDS study was sponsored by the NIH.

Balkan had no disclosures.

Study coauthors reported ties to Amgen and Novartis.

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A Small Step for Olive Oil as HFpEF Treatment

Extra virgin olive oil (EVOO) showed promise as a secondary prevention therapy for heart failure with preserved ejection fraction (HFpEF) in a small uncontrolled study.

Nine study participants with HFpEF and obesity were supplemented with unsaturated fatty acid-rich foods and had their EVOO intake estimated over 12 weeks according to their dietary recall, according to researchers led by Hayley Billingsley, RD, of Virginia Commonwealth University, who presented the data in a poster at this year’s virtual Heart Failure Society of American meeting.

Daily EVOO intake increased from zero at baseline to 23.6 g on average during the study, with greater EVOO consumption accompanied by small but significant improvements in cardiorespiratory fitness on cardiopulmonary exercise testing (CPET).

A statistical model indicated that a 40-g increase in EVOO intake led to increased peak VO2 by just under 2 mL/kg/min, a roughly 6% improvement compared with predicted peak VO2; oxygen uptake efficiency slope also increased by about 0.1.

The nine people in the study had a median age of 56 years. Five were women, and six people were Black.

Dietary recalls were conducted at baseline, 4, 8, and 12 week visits. Participants underwent CPET at baseline and at 12 weeks.

“Further studies are warranted to confirm this finding and establish a basis for testing the effect of EVOO on cardiorespiratory fitness as well as major cardiovascular outcomes and to explore these effects across differing baseline intakes of EVOO,” Billingsley said.

In particular, more work needs to be done with large, rigorous randomized trials, said Tariq Ahmad, MD, MPH, of Yale University School of Medicine, who was not involved with the study.

However, it is biologically plausible that EVOO may be beneficial for HFpEF, commented C. Noel Bairey Merz, MD, of Cedars-Sinai Medical Center in Los Angeles.

For example, olive oil is known to be high in monounsaturated fat, with lower levels of vitamin E, polyphenols, and lipid molecules that may contribute to its anti-inflammatory and antioxidant properties, one group recently cited from the literature.

Some consider HFpEF to be not one disease but several syndromes, some of which may be related to coronary microvascular dysfunction that is linked to inflammation.

If olive oil does help in HFpEF, it would be a source of hope for those with the condition, as patients currently have no treatments proven to improve their clinical outcomes. Results with sacubitril/valsartan (Entresto) have been mixed in this population, and other options have failed outright.

Ahmad noted a range of limitations to the study, such as lack of information on how patients were diagnosed, absence of a control group, and the small sample size.

Another point of caution is the known training effect in exercise studies, Bairey Merz said.

  • author['full_name']

    Nicole Lou is a reporter for MedPage Today, where she covers cardiology news and other developments in medicine. Follow


The study was supported by a grant from the NIH.

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