Cell-and molecular-level mechanisms contributing to diastolic dysfunction in HFpEF

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14 Scopus citations


Campbell KS, Sorrell VL. Cell-and molecular-level mechanisms contributing to diastolic dysfunction in HFpEF. J Appl Physiol 119: 1228-1232, 2015. First published April 24, 2015; doi:10.1152/japplphysiol.01168.2014.-Heart failure with preserved ejection fraction (HFpEF) is the default diagnosis for patients who have symptoms of heart failure, an ejection fraction >0.5, and evidence of diastolic dysfunction. The clinical condition, which was largely unrecognized 30 years ago, is now a major health problem and currently accounts for 50% of all patients with heart failure. Clinical studies show that patients with HFpEF exhibit increased passive stiffness of the ventricles and a slower rate of pressure decline during diastole. This review discusses some of the cell-and molecular-level mechanisms that contribute to these effects and focuses on data obtained using human samples. Collagen cross linking, modulation of protein kinase G-related pathways, Ca2+ handling, and strain-dependent detachment of cross bridges are highlighted as potential factors that could be modulated to improve ventricular function in patients with HFpEF.

Original languageEnglish
Pages (from-to)1228-1232
Number of pages5
JournalJournal of Applied Physiology
Issue number10
StatePublished - Nov 15 2015

Bibliographical note

Publisher Copyright:
© 2015 The American Physiological Society.


  • Heart failure
  • Myocardial stiffness
  • Myocardium
  • Myocyte
  • Ventricular function

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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