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Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction
Heart failure with preserved ejection fraction (HFpEF) is an increasingly studied entity accounting for 50% of all diagnosed heart failure and that has claimed its own dignity being markedly different from heart failure with reduced EF in terms of etiology and natural history (Graziani et al., 2018)...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848263/ https://www.ncbi.nlm.nih.gov/pubmed/31749710 http://dx.doi.org/10.3389/fphys.2019.01347 |
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author | D’Amario, Domenico Migliaro, Stefano Borovac, Josip A. Restivo, Attilio Vergallo, Rocco Galli, Mattia Leone, Antonio Maria Montone, Rocco A. Niccoli, Giampaolo Aspromonte, Nadia Crea, Filippo |
author_facet | D’Amario, Domenico Migliaro, Stefano Borovac, Josip A. Restivo, Attilio Vergallo, Rocco Galli, Mattia Leone, Antonio Maria Montone, Rocco A. Niccoli, Giampaolo Aspromonte, Nadia Crea, Filippo |
author_sort | D’Amario, Domenico |
collection | PubMed |
description | Heart failure with preserved ejection fraction (HFpEF) is an increasingly studied entity accounting for 50% of all diagnosed heart failure and that has claimed its own dignity being markedly different from heart failure with reduced EF in terms of etiology and natural history (Graziani et al., 2018). Recently, a growing body of evidence points the finger toward microvascular dysfunction as the major determinant of the pathological cascade that justifies clinical manifestations (Crea et al., 2017). The high burden of comorbidities such as metabolic syndrome, hypertension, atrial fibrillation, chronic kidney disease, obstructive sleep apnea, and similar, could lead to a systemic inflammatory state that impacts the physiology of the endothelium and the perivascular environment, engaging complex molecular pathways that ultimately converge to myocardial fibrosis, stiffening, and dysfunction (Paulus and Tschope, 2013). These changes could even self-perpetrate with a positive feedback where hypoxia and locally released inflammatory cytokines trigger interstitial fibrosis and hypertrophy (Ohanyan et al., 2018). Identifying microvascular dysfunction both as the cause and the maintenance mechanism of this condition has opened the field to explore specific pharmacological targets like nitric oxide (NO) pathway, sarcomeric titin, transforming growth factor beta (TGF-β) pathway, immunomodulators or adenosine receptors, trying to tackle the endothelial impairment that lies in the background of this syndrome (Graziani et al., 2018;Lam et al., 2018). Yet, many questions remain, and the new data collected still lack a translation to improved treatment strategies. To further elaborate on this tangled and exponentially growing topic, we will review the evidence favoring a microvasculature-driven etiology of this condition, its clinical correlations, the proposed diagnostic workup, and the available/hypothesized therapeutic options to address microvascular dysfunction in the failing heart. |
format | Online Article Text |
id | pubmed-6848263 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-68482632019-11-20 Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction D’Amario, Domenico Migliaro, Stefano Borovac, Josip A. Restivo, Attilio Vergallo, Rocco Galli, Mattia Leone, Antonio Maria Montone, Rocco A. Niccoli, Giampaolo Aspromonte, Nadia Crea, Filippo Front Physiol Physiology Heart failure with preserved ejection fraction (HFpEF) is an increasingly studied entity accounting for 50% of all diagnosed heart failure and that has claimed its own dignity being markedly different from heart failure with reduced EF in terms of etiology and natural history (Graziani et al., 2018). Recently, a growing body of evidence points the finger toward microvascular dysfunction as the major determinant of the pathological cascade that justifies clinical manifestations (Crea et al., 2017). The high burden of comorbidities such as metabolic syndrome, hypertension, atrial fibrillation, chronic kidney disease, obstructive sleep apnea, and similar, could lead to a systemic inflammatory state that impacts the physiology of the endothelium and the perivascular environment, engaging complex molecular pathways that ultimately converge to myocardial fibrosis, stiffening, and dysfunction (Paulus and Tschope, 2013). These changes could even self-perpetrate with a positive feedback where hypoxia and locally released inflammatory cytokines trigger interstitial fibrosis and hypertrophy (Ohanyan et al., 2018). Identifying microvascular dysfunction both as the cause and the maintenance mechanism of this condition has opened the field to explore specific pharmacological targets like nitric oxide (NO) pathway, sarcomeric titin, transforming growth factor beta (TGF-β) pathway, immunomodulators or adenosine receptors, trying to tackle the endothelial impairment that lies in the background of this syndrome (Graziani et al., 2018;Lam et al., 2018). Yet, many questions remain, and the new data collected still lack a translation to improved treatment strategies. To further elaborate on this tangled and exponentially growing topic, we will review the evidence favoring a microvasculature-driven etiology of this condition, its clinical correlations, the proposed diagnostic workup, and the available/hypothesized therapeutic options to address microvascular dysfunction in the failing heart. Frontiers Media S.A. 2019-11-05 /pmc/articles/PMC6848263/ /pubmed/31749710 http://dx.doi.org/10.3389/fphys.2019.01347 Text en Copyright © 2019 D’Amario, Migliaro, Borovac, Restivo, Vergallo, Galli, Leone, Montone, Niccoli, Aspromonte and Crea. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Physiology D’Amario, Domenico Migliaro, Stefano Borovac, Josip A. Restivo, Attilio Vergallo, Rocco Galli, Mattia Leone, Antonio Maria Montone, Rocco A. Niccoli, Giampaolo Aspromonte, Nadia Crea, Filippo Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title | Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title_full | Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title_fullStr | Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title_full_unstemmed | Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title_short | Microvascular Dysfunction in Heart Failure With Preserved Ejection Fraction |
title_sort | microvascular dysfunction in heart failure with preserved ejection fraction |
topic | Physiology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6848263/ https://www.ncbi.nlm.nih.gov/pubmed/31749710 http://dx.doi.org/10.3389/fphys.2019.01347 |
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