Exploring the potential relationship between collagen cross-linking and impaired myocardial relaxation in Marfan syndrome: An observational study using serum biomarkers.

Biomarker Diastolic function Echocardiography Left atrium Marfan syndrome Myocardial fibrosis Strain

Journal

International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291

Informations de publication

Date de publication:
01 Apr 2022
Historique:
received: 25 10 2021
revised: 16 01 2022
accepted: 24 01 2022
pubmed: 30 1 2022
medline: 15 3 2022
entrez: 29 1 2022
Statut: ppublish

Résumé

Increased collagen cross-linking (CCL) has been described in hypertensive cardiomyopathy by means of reduced serum ratio of serum carboxyterminal telopeptide of collagen type I (CITP) to matrix metalloproteinase-1 (MMP1). Previous studies have demonstrated the existence of primary impaired diastole in patients with Marfan syndrome (MFS), but little is known about the pathophysiology of this condition. 60 MFS patients (without previous cardiovascular surgery or significant valvular regurgitation) and 24 healthy controls (age and sex-matched) were enrolled. All participants underwent a comprehensive transthoracic echocardiographic study, including left atrial and left ventricular speckle-tracking strain analysis. CITP and MMP1 were measured in peripheral blood. All participants had normal diastolic function according to guidelines. Peak left atrial strain in the reservoir phase (LASr) was significantly reduced in the MFS cohort compared to controls (32.2 ± 9.4 vs 43.9 ± 7.0%; p < 0.001). Serum CITP and CITP:MMP1 ratio were lower among MFS patients, showing significant correlations with LASr (R = 0.311; p = 0.020 and R = 0.437; p = 0.001, respectively). The MFS cohort was divided into quartiles of LASr. MFS patients in the lowest quartile of LASr (<26%) had significantly lower values of CITP:MMP1 ratio compared to the other quartiles. The analysis of serum biomarkers revealed the presence of increased CCL in association with reduced LASr in the MFS cohort. Our results suggest that excessive CCL may play a role in the development of primary myocardial impairment in these patients. Future studies are needed to confirm our findings and evaluate the prognostic role of CCL markers in the MFS population.

Sections du résumé

BACKGROUND BACKGROUND
Increased collagen cross-linking (CCL) has been described in hypertensive cardiomyopathy by means of reduced serum ratio of serum carboxyterminal telopeptide of collagen type I (CITP) to matrix metalloproteinase-1 (MMP1). Previous studies have demonstrated the existence of primary impaired diastole in patients with Marfan syndrome (MFS), but little is known about the pathophysiology of this condition.
METHODS METHODS
60 MFS patients (without previous cardiovascular surgery or significant valvular regurgitation) and 24 healthy controls (age and sex-matched) were enrolled. All participants underwent a comprehensive transthoracic echocardiographic study, including left atrial and left ventricular speckle-tracking strain analysis. CITP and MMP1 were measured in peripheral blood.
RESULTS RESULTS
All participants had normal diastolic function according to guidelines. Peak left atrial strain in the reservoir phase (LASr) was significantly reduced in the MFS cohort compared to controls (32.2 ± 9.4 vs 43.9 ± 7.0%; p < 0.001). Serum CITP and CITP:MMP1 ratio were lower among MFS patients, showing significant correlations with LASr (R = 0.311; p = 0.020 and R = 0.437; p = 0.001, respectively). The MFS cohort was divided into quartiles of LASr. MFS patients in the lowest quartile of LASr (<26%) had significantly lower values of CITP:MMP1 ratio compared to the other quartiles.
CONCLUSIONS CONCLUSIONS
The analysis of serum biomarkers revealed the presence of increased CCL in association with reduced LASr in the MFS cohort. Our results suggest that excessive CCL may play a role in the development of primary myocardial impairment in these patients. Future studies are needed to confirm our findings and evaluate the prognostic role of CCL markers in the MFS population.

Identifiants

pubmed: 35092759
pii: S0167-5273(22)00176-0
doi: 10.1016/j.ijcard.2022.01.050
pii:
doi:

Substances chimiques

Biomarkers 0
Collagen Type I 0

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

125-130

Informations de copyright

Copyright © 2022 Elsevier B.V. All rights reserved.

Auteurs

Eusebio García-Izquierdo (E)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain. Electronic address: usegij@gmail.com.

Susana Mingo-Santos (S)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Consuelo Olivo-Rodríguez (C)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Vanessa Moñivas-Palomero (V)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Mercedes Rivas-Lasarte (M)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Carlos E Martín-López (CE)

Department of Cardiac Surgery, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Silvia Rosado-García (S)

Biobank, IDIPHISA, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Antonio J Sánchez-López (AJ)

Biobank, IDIPHISA, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Juan Miguel Redondo (JM)

Centro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Spain, Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.

Fernando Rodríguez-Pascual (F)

Centro de Biología Molecular "Severo Ochoa", CSIC-Universidad Autónoma de Madrid (UAM), Madrid, Spain.

Javier Segovia-Cubero (J)

Department of Cardiology, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

Alberto Forteza-Gil (A)

Department of Cardiac Surgery, Hospital Universitario Puerta de Hierro Majadahonda, Madrid, Spain.

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Classifications MeSH