Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning

Swine subjected to 2 weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but left ventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardial remodeling characterized by myocyte hypertrophy and interstitial fibrosis led to a...

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Detalles Bibliográficos
Autores principales: Weil, Brian R., Techiryan, George, Suzuki, Gen, Konecny, Filip, Canty, John M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier 2019
Materias:
PRECLINICAL RESEARCH
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6712414/
https://www.ncbi.nlm.nih.gov/pubmed/31468008
http://dx.doi.org/10.1016/j.jacbts.2019.04.002
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author Weil, Brian R.
Techiryan, George
Suzuki, Gen
Konecny, Filip
Canty, John M.
author_facet Weil, Brian R.
Techiryan, George
Suzuki, Gen
Konecny, Filip
Canty, John M.
author_sort Weil, Brian R.
collection PubMed
description Swine subjected to 2 weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but left ventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardial remodeling characterized by myocyte hypertrophy and interstitial fibrosis led to a marked reduction in LV diastolic compliance, which protected the heart from stretch-induced myocyte injury and preserved LV ejection fraction without anatomic LV hypertrophy. These results support a novel paradigm that links cardiac adaptations to RPO with the pathogenesis of reduced LV diastolic compliance and may explain how LV stiffening can occur in the absence of sustained hypertension or anatomic hypertrophy.
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spelling pubmed-67124142019-08-29 Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning Weil, Brian R. Techiryan, George Suzuki, Gen Konecny, Filip Canty, John M. JACC Basic Transl Sci PRECLINICAL RESEARCH Swine subjected to 2 weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but left ventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardial remodeling characterized by myocyte hypertrophy and interstitial fibrosis led to a marked reduction in LV diastolic compliance, which protected the heart from stretch-induced myocyte injury and preserved LV ejection fraction without anatomic LV hypertrophy. These results support a novel paradigm that links cardiac adaptations to RPO with the pathogenesis of reduced LV diastolic compliance and may explain how LV stiffening can occur in the absence of sustained hypertension or anatomic hypertrophy. Elsevier 2019-08-26 /pmc/articles/PMC6712414/ /pubmed/31468008 http://dx.doi.org/10.1016/j.jacbts.2019.04.002 Text en © 2019 The Authors http://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle PRECLINICAL RESEARCH
Weil, Brian R.
Techiryan, George
Suzuki, Gen
Konecny, Filip
Canty, John M.
Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title_full Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title_fullStr Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title_full_unstemmed Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title_short Adaptive Reductions in Left Ventricular Diastolic Compliance Protect the Heart From Stretch-Induced Stunning
title_sort adaptive reductions in left ventricular diastolic compliance protect the heart from stretch-induced stunning
topic PRECLINICAL RESEARCH
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6712414/
https://www.ncbi.nlm.nih.gov/pubmed/31468008
http://dx.doi.org/10.1016/j.jacbts.2019.04.002
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