The Cardiomyocyte in Heart Failure with Preserved Ejection Fraction-Victim of Its Environment?

Angela Rocca1, Ruud B van Heeswijk2, Jonas Richiardi2

  • 1Department of Cardiology, Faculty of Biology and Medicine, Lausanne University Hospital, University of Lausanne, 1011 Lausanne, Switzerland.

Cells
|March 10, 2022
PubMed

Insights

Heart failure with preserved ejection fraction (HFpEF) is common, yet effective treatments are lacking due to poor understanding of its causes. This review integrates animal model and human data to identify new therapeutic targets for HFpEF.

Area of Science:

  • Cardiology
  • Pathophysiology
  • Translational Medicine

Background:

  • Heart failure with preserved ejection fraction (HFpEF) is increasingly prevalent, representing the majority of heart failure cases.
  • Current medical therapies lack efficacy in improving cardiovascular outcomes for HFpEF patients, highlighting a significant unmet clinical need.
  • The heterogeneity of HFpEF patients and incomplete understanding of its pathophysiology hinder the development of effective treatments.

Purpose of the Study:

  • To review and synthesize current knowledge on HFpEF pathophysiology, integrating findings from animal models and human studies.
  • To explore the role of comorbidities in HFpEF and their impact on cellular mechanisms.
  • To identify potential new therapeutic targets by bridging the gap between cardiomyocyte pathophysiology and clinical observations.

Main Methods:

  • Literature review integrating data from animal models of HFpEF and human clinical studies.
  • Analysis of cellular pathophysiology and the role of comorbidities in HFpEF.
  • Synthesis of observational data to connect molecular mechanisms with clinical manifestations.

Main Results:

  • Animal models have provided novel insights into the cellular pathophysiology of HFpEF, particularly concerning the role of prevalent comorbidities.
  • Evidence suggests that previously overlooked cellular mechanisms contribute to HFpEF.
  • A convergence of cardiomyocyte-focused research and clinical data is emerging.

Conclusions:

  • A deeper understanding of HFpEF pathophysiology, informed by animal models and human data, is crucial for developing effective therapies.
  • Targeting cellular mechanisms and considering the impact of comorbidities may lead to new therapeutic strategies for HFpEF.
  • Further research integrating basic science and clinical findings holds promise for improving outcomes in HFpEF patients.

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