期刊
CELLS
卷 9, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/cells9010242
关键词
heart failure with preserved ejection fraction; heart failure with reduced ejection fraction; inflammation; endothelial dysfunction; cardiomyocyte alterations
类别
资金
- European Research Area Networks on Cardiovascular Diseases (ERA-CVD) [LYMIT-DIS, 2016]
- FondsWetenschappelijk Onderzoek [1160718N, 9091018N, G091018N]
- ERA-Net-CVD project MacroERA [2016] [01KL1706]
- IMI2-CARDIATEAM [821508]
- Netherlands Cardiovascular Research Initiative
- Dutch Heart Foundation, CVON2016-Early HFPEF [2015-10]
- Dutch Heart Foundation, CVON She-PREDICTS, grant 2017-21
- Dutch Heart Foundation, CVON Arena-PRIME
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.
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