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dc.creatorMiranda-Silva, D. (Daniela)-
dc.creatorGonçalves-Rodrigues, P. (Patrícia)-
dc.creatorAlmeida-Coelho, J. (João)-
dc.creatorHamdani, N. (Nazha)-
dc.creatorLima, T. (Tania)-
dc.creatorConceição, G. (Glória)-
dc.creatorSousa-Mendes, C. (Cláudia)-
dc.creatorMoura, C. (Cláudia)-
dc.creatorGonzalez, A. (Arantxa)-
dc.creatorDiez-Martinez, J. (Javier)-
dc.creatorLinke, W.A. (Wolfgang A.)-
dc.creatorLeite-Moreira, A. (Adelino)-
dc.creatorFalcão-Pires, I. (Ines)-
dc.identifier.citationMiranda-Silva, D. (Daniela); Gonçalves-Rodrigues, P. (Patrícia); Almeida-Coelho, J. (João); et al. "Characterization of biventricular alterations in myocardial (reverse) remodelling in aortic bandinginduced chronic pressure overload". Scientific Reports. 9 (2956), 2019, 1 - 14es
dc.identifier.otherPMID: 30814653-
dc.description.abstractAortic Stenosis (AS) is the most frequent valvulopathy in the western world. Traditionally aortic valve replacement (AVR) has been recommended immediately after the onset of heart failure (HF) symptoms. However, recent evidence suggests that AVR outcome can be improved if performed earlier. After AVR, the process of left ventricle (LV) reverse remodelling (RR) is variable and frequently incomplete. In this study, we aimed at detecting mechanism underlying the process of LV RR regarding myocardial structural, functional and molecular changes before the onset of HF symptoms. Wistar-Han rats were subjected to 7-weeks of ascending aortic-banding followed by a 2-week period of debanding to resemble AS-induced LV remodelling and the early events of AVR-induced RR, respectively. This resulted in 3 groups: Sham (n = 10), Banding (Ba, n = 15) and Debanding (Deb, n = 10). Concentric hypertrophy and diastolic dysfunction (DD) were patent in the Ba group. Aortic-debanding induced RR, which promoted LV functional recovery, while cardiac structure did not normalise. Cardiac parameters of RV dysfunction, assessed by echocardiography and at the cardiomyocyte level prevailed altered after debanding. After debanding, these alterations were accompanied by persistent changes in pathways associated to myocardial hypertrophy, fibrosis and LV inflammation. Aortic banding induced pulmonary arterial wall thickness to increase and correlates negatively with effort intolerance and positively with E/e' and left atrial area. We described dysregulated pathways in LV and RV remodelling and RR after AVR. Importantly we showed important RV-side effects of aortic constriction, highlighting the impact that LV-reverse remodelling has on both ventricles.es_ES
dc.description.sponsorshipTis project is supported by Fundo Europeu de Desenvolvimento Regional (FEDER) through Compete 2020 – Programa Operacional Competitividade E Internacionalização (POCI), the project DOCNET (norte01-0145-feder-000003), supported by Norte Portugal regional operational programme (norte 2020), under the Portugal 2020 partnership agreement, through the European Regional Development Fund (ERDF), the project NETDIAMOND (POCI-01-0145-FEDER-016385), supported by European Structural And Investment Funds, Lisbon’s regional operational program 2020. Daniela Miranda Silva and Patrícia Rodrigues are funded by Fundação para a Ciência e Tecnologia (FCT) by fellowship grants (SFRH/BD/87556/2012 and SFRH/ BD/96026/2013 respectively) and Glória Conceição is funded by FSE – European Social Fund through Regional Operational Programme (Norte 2020).es_ES
dc.publisherSpringer Science and Business Media LLCes_ES
dc.subjectMaterias Investigacion::Ciencias de la Salud::Cardiologíaes_ES
dc.titleCharacterization of biventricular alterations in myocardial (reverse) remodelling in aortic bandinginduced chronic pressure overloades_ES
dc.description.noteThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were madees_ES
dadun.citation.publicationNameScientific Reportses_ES

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