Abstract
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 language | English |
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Pages (from-to) | 1228-1232 |
Number of pages | 5 |
Journal | Journal of Applied Physiology |
Volume | 119 |
Issue number | 10 |
DOIs | |
State | Published - Nov 15 2015 |
Bibliographical note
Publisher Copyright:© 2015 The American Physiological Society.
Keywords
- Heart failure
- Myocardial stiffness
- Myocardium
- Myocyte
- Ventricular function
ASJC Scopus subject areas
- Physiology
- Physiology (medical)