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

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          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.

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          Most cited references145

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          The global health and economic burden of hospitalizations for heart failure: lessons learned from hospitalized heart failure registries.

          Heart failure is a global pandemic affecting an estimated 26 million people worldwide and resulting in more than 1 million hospitalizations annually in both the United States and Europe. Although the outcomes for ambulatory HF patients with a reduced ejection fraction (EF) have improved with the discovery of multiple evidence-based drug and device therapies, hospitalized heart failure (HHF) patients continue to experience unacceptably high post-discharge mortality and readmission rates that have not changed in the last 2 decades. In addition, the proportion of HHF patients classified as having a preserved EF continues to grow and may overtake HF with a reduced EF in the near future. However, the prognosis for HF with a preserved EF is similar and there are currently no available disease-modifying therapies. HHF registries have significantly improved our understanding of this clinical entity and remain an important source of data shaping both public policy and research efforts. The authors review global HHF registries to describe the patient characteristics, management, outcomes and their predictors, quality improvement initiatives, regional differences, and limitations of the available data. Moreover, based on the lessons learned, they also propose a roadmap for the design and conduct of future HHF registries. Copyright © 2014 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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            Cardiac Fibrosis: The Fibroblast Awakens.

            Myocardial fibrosis is a significant global health problem associated with nearly all forms of heart disease. Cardiac fibroblasts comprise an essential cell type in the heart that is responsible for the homeostasis of the extracellular matrix; however, upon injury, these cells transform to a myofibroblast phenotype and contribute to cardiac fibrosis. This remodeling involves pathological changes that include chamber dilation, cardiomyocyte hypertrophy and apoptosis, and ultimately leads to the progression to heart failure. Despite the critical importance of fibrosis in cardiovascular disease, our limited understanding of the cardiac fibroblast impedes the development of potential therapies that effectively target this cell type and its pathological contribution to disease progression. This review summarizes current knowledge regarding the origins and roles of fibroblasts, mediators and signaling pathways known to influence fibroblast function after myocardial injury, as well as novel therapeutic strategies under investigation to attenuate cardiac fibrosis.
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              Coronary microvascular rarefaction and myocardial fibrosis in heart failure with preserved ejection fraction.

              Characterization of myocardial structural changes in heart failure with preserved ejection fraction (HFpEF) has been hindered by the limited availability of human cardiac tissue. Cardiac hypertrophy, coronary artery disease (CAD), coronary microvascular rarefaction, and myocardial fibrosis may contribute to HFpEF pathophysiology.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Cells
                Cells
                cells
                Cells
                MDPI
                2073-4409
                18 January 2020
                January 2020
                : 9
                : 1
                : 242
                Affiliations
                [1 ]Center for Molecular and Vascular Biology, KU Leuven, Herestraat 49, bus 911, 3000 Leuven, Belgium; steven.simmonds@ 123456kuleuven.be (S.J.S.); ilona.cuijpers@ 123456kuleuven.be (I.C.); s.heymans@ 123456maastrichtuniversity.nl (S.H.)
                [2 ]Department of Cardiology, Cardiovascular Research Institute (CARIM), Maastricht University Medical Centre, Universiteitssingel 50, 6229 ER Maastricht, The Netherlands
                [3 ]Netherlands Heart Institute, Holland Heart House, Moreelsepark 1, 3511 Utrecht, The Netherlands
                [4 ]William Harvey Research Institute, Barts Heart Centre, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK
                Author notes
                [* ]Correspondence: liz.jones@ 123456kuleuven.be ; Tel.: +32-16345775
                [†]

                These authors contributed equally to this work.

                Author information
                https://orcid.org/0000-0001-8163-1573
                Article
                cells-09-00242
                10.3390/cells9010242
                7016826
                31963679
                52201975-512d-4a8d-863a-c4067c676ea1
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 23 December 2019
                : 15 January 2020
                Categories
                Review

                heart failure with preserved ejection fraction,heart failure with reduced ejection fraction,inflammation,endothelial dysfunction,cardiomyocyte alterations

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