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Postsystolic thickening is a potential new clinical sign of injured myocardium in marfan syndrome.
Mas-Stachurska, Aleksandra; Egea, Gustavo; de Bruin-Bon, Rianne; Rudenick, Paula; Sanchis, Laura; Bouma, Berto J; Mulder, Barbara J; Bijnens, Bart; Sitges, Marta.
Afiliação
  • Mas-Stachurska A; Cardiovascular Institute, Hospital Clinic, University of Barcelona and Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS); CERCA Programme/Generalitat de Catalunya, Barcelona, Spain. astachur@gmail.com.
  • Egea G; Institut Hospital del Mar d'Investigacions Mèdiques (IMIM), Barcelona, Spain. astachur@gmail.com.
  • de Bruin-Bon R; Department of Biomedical Sciences, University of Barcelona School of Medicine and Health Sciences and Institut d'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS), Barcelona, Spain.
  • Rudenick P; Cardiology Department, Amsterdam University Medical Centers, Location Academic Medic Centrum, Amsterdam, The Netherlands.
  • Sanchis L; ICREA, Barcelona, Spain.
  • Bouma BJ; Cardiovascular Institute, Hospital Clinic, University of Barcelona and Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS); CERCA Programme/Generalitat de Catalunya, Barcelona, Spain.
  • Mulder BJ; Cardiology Department, Amsterdam University Medical Centers, Location Academic Medic Centrum, Amsterdam, The Netherlands.
  • Bijnens B; Cardiology Department, Amsterdam University Medical Centers, Location Academic Medic Centrum, Amsterdam, The Netherlands.
  • Sitges M; Cardiovascular Institute, Hospital Clinic, University of Barcelona and Institut D'Investigacions Biomèdiques August Pi I Sunyer (IDIBAPS); CERCA Programme/Generalitat de Catalunya, Barcelona, Spain.
Sci Rep ; 11(1): 15790, 2021 08 04.
Article em En | MEDLINE | ID: mdl-34349174
The mechanisms leading to cardiac remodeling in Marfan syndrome (MFS) are a matter of debate since it could be either due to structural dysfunction of the myocardial extracellular matrix or to increased afterload caused by the dilated aorta. We aim to characterize the presence of abnormal myocardial function in MFS and to investigate its potential association with increased afterload. Aorta, left ventricle (LV) and the postsystolic thickening (PST) were analyzed in echocardiography in Fbn1C1039G/+ mice and in patients with MFS in comparison with wild type (WT) mice and healthy humans. PST was more frequent in MFS than in WT mice (p < 0.05). MFS mice with PST showed larger aorta than those without PST. Patients with MFS showed larger aorta, poorer LV function and a higher prevalence of PST (56%) than did the healthy controls (23%); p = 0.003. Blood pressure was similar. The higher prevalence of PST in an experimental murine model and in MFS patients, regardless of systemic arterial pressure, suggests an increased afterload on the LV myocardium. This finding supports the use of PST as an indicator of myocardial damage and encourage searching for novel early preventive therapy.
Assuntos

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Síndrome de Marfan / Miocárdio Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals / Humans Idioma: En Revista: Sci Rep Ano de publicação: 2021 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Síndrome de Marfan / Miocárdio Tipo de estudo: Prognostic_studies / Risk_factors_studies Limite: Animals / Humans Idioma: En Revista: Sci Rep Ano de publicação: 2021 Tipo de documento: Article