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Diastolic myofilament dysfunction in the failing human heart

In recent years, it has become evident that heart failure is not solely due to reduced contractile performance of the heart muscle as impaired relaxation is evident in almost all heart failure patients. In more than half of all heart failure patients, diastolic dysfunction is the major cardiac defic...

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Autor principal: van der Velden, Jolanda
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2011
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114087/
https://www.ncbi.nlm.nih.gov/pubmed/21487693
http://dx.doi.org/10.1007/s00424-011-0960-3
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author van der Velden, Jolanda
author_facet van der Velden, Jolanda
author_sort van der Velden, Jolanda
collection PubMed
description In recent years, it has become evident that heart failure is not solely due to reduced contractile performance of the heart muscle as impaired relaxation is evident in almost all heart failure patients. In more than half of all heart failure patients, diastolic dysfunction is the major cardiac deficit. These heart failure patients have normal (or preserved) left ventricular ejection fraction, but impaired diastolic function evident from increased left ventricular end-diastolic pressure. Perturbations at the cellular level which cause impaired relaxation of the heart muscle involve changes in Ca(2+)-handling proteins, extracellular matrix components, and myofilament properties. The present review discusses the deficits in myofilament function observed in human heart failure and the most likely underlying causal protein changes. Moreover, the consequences of impaired myofilament function for in vivo diastolic dysfunction are discussed taking into account the reported changes in Ca(2+) handling.
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spelling pubmed-31140872011-07-14 Diastolic myofilament dysfunction in the failing human heart van der Velden, Jolanda Pflugers Arch Invited Review In recent years, it has become evident that heart failure is not solely due to reduced contractile performance of the heart muscle as impaired relaxation is evident in almost all heart failure patients. In more than half of all heart failure patients, diastolic dysfunction is the major cardiac deficit. These heart failure patients have normal (or preserved) left ventricular ejection fraction, but impaired diastolic function evident from increased left ventricular end-diastolic pressure. Perturbations at the cellular level which cause impaired relaxation of the heart muscle involve changes in Ca(2+)-handling proteins, extracellular matrix components, and myofilament properties. The present review discusses the deficits in myofilament function observed in human heart failure and the most likely underlying causal protein changes. Moreover, the consequences of impaired myofilament function for in vivo diastolic dysfunction are discussed taking into account the reported changes in Ca(2+) handling. Springer-Verlag 2011-04-13 2011 /pmc/articles/PMC3114087/ /pubmed/21487693 http://dx.doi.org/10.1007/s00424-011-0960-3 Text en © The Author(s) 2011 https://creativecommons.org/licenses/by-nc/4.0/ This article is distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the original author(s) and source are credited.
spellingShingle Invited Review
van der Velden, Jolanda
Diastolic myofilament dysfunction in the failing human heart
title Diastolic myofilament dysfunction in the failing human heart
title_full Diastolic myofilament dysfunction in the failing human heart
title_fullStr Diastolic myofilament dysfunction in the failing human heart
title_full_unstemmed Diastolic myofilament dysfunction in the failing human heart
title_short Diastolic myofilament dysfunction in the failing human heart
title_sort diastolic myofilament dysfunction in the failing human heart
topic Invited Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3114087/
https://www.ncbi.nlm.nih.gov/pubmed/21487693
http://dx.doi.org/10.1007/s00424-011-0960-3
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