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Background <p>The prevalence of heart failure with preserved systolic ejection fraction (HFpEF) is continually increasing and accounts for a&#xa0;substantial proportion of all cases of heart failure. Pathophysiologically, this is particularly characterized by diastolic dysfunction and the factors involved in the formation are still the subject of current research. Promising treatment approaches with confirmed clinical benefits in HFpEF are so far limited.</p> Method <p>A&#xa0;selective literature search was carried out in PubMed with the keywords HFpEF, heart failure, HFA-PEFF and cardiac resynchronization treatment. The search period included publications from 2000–2025. To reduce methodical bias guidelines, randomized controlled studies, meta-analyses and clinical register studies were predominantly considered. Studies with only heart failure with reduced (HFrEF) or moderately reduced (HFmrEF) ejection fraction populations and publications without defined HFpEF criteria were excluded.</p> Results <p>Many of the randomized controlled studies on different pharmacological treatment approaches failed to achieve their primary endpoints in patients with HFpEF, particularly with respect to mortality and cardiovascular events. Modern sodium-glucose transporter&#xa0;2 (SGLT-2) inhibitors have shown to be a&#xa0;very promising treatment approach in studies and are therefore recommended by the European Society of Cardiology (ESC) for treatment of HFpEF (evidence level&#xa0;A). Further studies with glucagon-like peptide&#xa0;1 (GLP-1) agonists and finerenone could also document a&#xa0;significant improvement of some clinical endpoints, such as a&#xa0;lower hospitalization rate.</p> Conclusion <p>A&#xa0;pathophysiological clarification of the cause and treatment of HFpEF requires intensive research. Future treatment strategies should concentrate more strongly on the comorbidities of the patients to cope with the heterogeneous disease mechanisms of HFpEF.</p>

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Diagnostik und Therapieansätze der Herzinsuffizienz mit erhaltener systolischer Funktion

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月10日

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  • Mathilde Beyer,
  • Andreas Mügge,
  • Ibrahim Akin,
  • Loek van Heerebeek,
  • Ibrahim El-Battrawy,
  • Nazha Hamdani

摘要

Background

The prevalence of heart failure with preserved systolic ejection fraction (HFpEF) is continually increasing and accounts for a substantial proportion of all cases of heart failure. Pathophysiologically, this is particularly characterized by diastolic dysfunction and the factors involved in the formation are still the subject of current research. Promising treatment approaches with confirmed clinical benefits in HFpEF are so far limited.

Method

A selective literature search was carried out in PubMed with the keywords HFpEF, heart failure, HFA-PEFF and cardiac resynchronization treatment. The search period included publications from 2000–2025. To reduce methodical bias guidelines, randomized controlled studies, meta-analyses and clinical register studies were predominantly considered. Studies with only heart failure with reduced (HFrEF) or moderately reduced (HFmrEF) ejection fraction populations and publications without defined HFpEF criteria were excluded.

Results

Many of the randomized controlled studies on different pharmacological treatment approaches failed to achieve their primary endpoints in patients with HFpEF, particularly with respect to mortality and cardiovascular events. Modern sodium-glucose transporter 2 (SGLT-2) inhibitors have shown to be a very promising treatment approach in studies and are therefore recommended by the European Society of Cardiology (ESC) for treatment of HFpEF (evidence level A). Further studies with glucagon-like peptide 1 (GLP-1) agonists and finerenone could also document a significant improvement of some clinical endpoints, such as a lower hospitalization rate.

Conclusion

A pathophysiological clarification of the cause and treatment of HFpEF requires intensive research. Future treatment strategies should concentrate more strongly on the comorbidities of the patients to cope with the heterogeneous disease mechanisms of HFpEF.