Kinetics of selected serum markers of fibrosis in patients with dilated cardiomyopathy and different grades of diastolic dysfunction of the left ventricle.


Journal

Cardiology journal
ISSN: 1898-018X
Titre abrégé: Cardiol J
Pays: Poland
ID NLM: 101392712

Informations de publication

Date de publication:
2020
Historique:
received: 13 07 2018
accepted: 08 11 2018
revised: 09 10 2018
pubmed: 30 11 2018
medline: 18 9 2021
entrez: 29 11 2018
Statut: ppublish

Résumé

Fibrosis of the extracellular matrix (ECM) in dilated cardiomyopathy (DCM) is common and compromises both systolic and diastolic function. The aim of this study was to investigate the kinetics of ECM fibrosis markers over a 12 month follow-up in patients with DCM based on the severity of diastolic dysfunction (DD). Seventy consecutive DCM patients (48 ± 12.1 years, ejection fraction 24.4 ± 7.4%) were included in the study. The grade of DD was determined using the ASE/EACVI algorithm. Markers of ECM fibrosis were measured at baseline and at 3 and 12 month follow-ups: collagen type I and III (PICP, PINP, PIIICP, PIIINP), transforming growth factor beta-1 (TGF1-b), connective tissue growth factor (CTGF) and galectin-3 were measured. Patients were divided into three groups according to DD severity: 30 patients with grade I, 18 with grade II and 22 with grade III of DD. Levels of PICP, PINP were increased over a 12-month period, while PIIINP decreased and PIIICP unchanged. Levels of TGF1-b decreased from the 3 to the 12-month points in grade I and II DD, and in grade III they remained unchanged. Levels of CTGF decreased over 12 months in grade III DD but were unchanged in grades I and II. Galectin-3 levels remained the same over all observation periods, irrespective of DD grade. Regardless of the DD grade, markers of collagen type I synthesis increased, markers of collagen type III decreased. Levels of TGF and CTGF had a tendency to decrease. Galectin-3 was revealed not to be a marker discriminating the severity of DD.

Sections du résumé

BACKGROUND
Fibrosis of the extracellular matrix (ECM) in dilated cardiomyopathy (DCM) is common and compromises both systolic and diastolic function. The aim of this study was to investigate the kinetics of ECM fibrosis markers over a 12 month follow-up in patients with DCM based on the severity of diastolic dysfunction (DD).
METHODS
Seventy consecutive DCM patients (48 ± 12.1 years, ejection fraction 24.4 ± 7.4%) were included in the study. The grade of DD was determined using the ASE/EACVI algorithm. Markers of ECM fibrosis were measured at baseline and at 3 and 12 month follow-ups: collagen type I and III (PICP, PINP, PIIICP, PIIINP), transforming growth factor beta-1 (TGF1-b), connective tissue growth factor (CTGF) and galectin-3 were measured.
RESULTS
Patients were divided into three groups according to DD severity: 30 patients with grade I, 18 with grade II and 22 with grade III of DD. Levels of PICP, PINP were increased over a 12-month period, while PIIINP decreased and PIIICP unchanged. Levels of TGF1-b decreased from the 3 to the 12-month points in grade I and II DD, and in grade III they remained unchanged. Levels of CTGF decreased over 12 months in grade III DD but were unchanged in grades I and II. Galectin-3 levels remained the same over all observation periods, irrespective of DD grade.
CONCLUSIONS
Regardless of the DD grade, markers of collagen type I synthesis increased, markers of collagen type III decreased. Levels of TGF and CTGF had a tendency to decrease. Galectin-3 was revealed not to be a marker discriminating the severity of DD.

Identifiants

pubmed: 30484268
pii: VM/OJS/J/59268
doi: 10.5603/CJ.a2018.0143
pmc: PMC8079113
doi:

Substances chimiques

Biomarkers 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

726-734

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Auteurs

Sylwia Wiśniowska-Śmiałek (S)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland. swisniowskasmialek@gmail.com.

Ewa Dziewięcka (E)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Katarzyna Holcman (K)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Ewa Wypasek (E)

Department of Molecular Biology, John Paul II Hospital, Krakow, Poland, ul. Prądnicka 80, 31-202 Cracow, Poland.

Lusine Khachatryan (L)

Jagiellonian University, Medical Collage, Krakow, Poland, ul. Św. Anny 12, 31-008 Cracow, Poland.

Aleksandra Karabinowska (A)

Jagiellonian University, Medical Collage, Krakow, Poland, ul. Św. Anny 12, 31-008 Cracow, Poland.

Maria Szymonowicz (M)

Jagiellonian University, Medical Collage, Krakow, Poland, ul. Św. Anny 12, 31-008 Cracow, Poland.

Agata Leśniak-Sobelga (A)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Marta Hlawaty (M)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Magdalena Kostkiewicz (M)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Piotr Podolec (P)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

Paweł Rubiś (P)

Collegium Medicum of Jagiellonian University, Department of Cardiac and Vascular Diseases, John Paul II Hospital, Kraków, Poland, ul.Prądnicka 80, 31-202 Cracow, Poland.

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