Cellular and Molecular Differences between HFpEF and HFrEF: A Step Ahead in an Improved Pathological Understanding

Steven J. Simmonds, Ilona Cuijpers, Stephane Heymans, Elizabeth A. V. Jones*

*Corresponding author for this work

Research output: Contribution to journal(Systematic) Review article peer-review

Abstract

Heart failure (HF) is the most rapidly growing cardiovascular health burden worldwide. HF can be classified into three groups based on the percentage of the ejection fraction (EF): heart failure with reduced EF (HFrEF), heart failure with mid-range-also called mildly reduced EF- (HFmrEF), and heart failure with preserved ejection fraction (HFpEF). HFmrEF can progress into either HFrEF or HFpEF, but its phenotype is dominated by coronary artery disease, as in HFrEF. HFrEF and HFpEF present with differences in both the development and progression of the disease secondary to changes at the cellular and molecular level. While recent medical advances have resulted in efficient and specific treatments for HFrEF, these treatments lack efficacy for HFpEF management. These differential response rates, coupled to increasing rates of HF, highlight the significant need to understand the unique pathogenesis of HFrEF and HFpEF. In this review, we summarize the differences in pathological development of HFrEF and HFpEF, focussing on disease-specific aspects of inflammation and endothelial function, cardiomyocyte hypertrophy and death, alterations in the giant spring titin, and fibrosis. We highlight the areas of difference between the two diseases with the aim of guiding research efforts for novel therapeutics in HFrEF and HFpEF.

Original languageEnglish
Article number242
Number of pages22
JournalCells
Volume9
Issue number1
DOIs
Publication statusPublished - Jan 2020

Keywords

  • heart failure with preserved ejection fraction
  • heart failure with reduced ejection fraction
  • inflammation
  • endothelial dysfunction
  • cardiomyocyte alterations
  • PRESERVED EJECTION FRACTION
  • ENDOTHELIUM-DEPENDENT VASODILATION
  • VENTRICULAR DIASTOLIC FUNCTION
  • ACUTE MYOCARDIAL-INFARCTION
  • FIBRILLAR COLLAGEN CONTENT
  • SMOOTH-MUSCLE-CELLS
  • ONSET HEART-FAILURE
  • SARCOPLASMIC-RETICULUM
  • OXIDATIVE STRESS
  • TITIN ISOFORM

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