Prediction of Left Ventricular Reverse Remodeling and Outcomes by Circulating Collagen-Derived Peptides.

heart failure left ventricular ejection fraction left ventricular reverse remodeling outcomes procollagen type-I C-terminal propeptide

Journal

JACC. Heart failure
ISSN: 2213-1787
Titre abrégé: JACC Heart Fail
Pays: United States
ID NLM: 101598241

Informations de publication

Date de publication:
01 2023
Historique:
received: 21 03 2022
revised: 04 08 2022
accepted: 01 09 2022
entrez: 4 1 2023
pubmed: 5 1 2023
medline: 7 1 2023
Statut: ppublish

Résumé

Myocardial fibrosis may increase vulnerability to poor prognosis in patients with heart failure (HF), even in those patients exhibiting left ventricular reverse remodeling (LVRR) after guideline-based therapies. This study sought to characterize fibrosis at baseline in patients with HF with left ventricular ejection fraction (LVEF) <50% by determining serum collagen type I-derived peptides (procollagen type I C-terminal propeptide [PICP] and ratio of collagen type I C-terminal telopeptide to matrix metalloproteinase-1) and to evaluate their association with LVRR and prognosis. Peptides were determined in 1,034 patients with HF at baseline. One-year echocardiography was available in 665 patients. Associations of peptides with 1-year changes in echocardiographic variables were analyzed by multivariable linear mixed models. LVEF was considered improved if it increased by ≥15% or to ≥50% or if it increased by ≥10% to >40% in patients with LVEF ≤40%. Cardiovascular death and HF-related outcomes were analyzed in all patients randomized to derivation (n = 648) and validation (n = 386) cohorts. Continuous associations with echocardiographic changes were observed only for PICP. Compared with high-PICP (≥108.1 ng/mL) patients, low-PICP (<108.1 ng/mL) patients exhibited enhanced LVRR and a lower risk of HF-related outcomes (P ≤ 0.018), with women and nonischemic patients with HF showing a stronger LVEF increase (interaction P ≤ 0.010). LVEF increase was associated with a better prognosis, particularly in low-PICP patients (interaction P ≤ 0.029). Only patients with both low PICP and improved LVEF exhibited a better clinical evolution than patients with nonimproved LVEF (P < 0.001). Phenotyping with PICP, a peptide associated with myocardial fibrosis, may be useful to differentiate patients with HF who are more likely to experience clinical myocardial recovery from those with partial myocardial improvement.

Sections du résumé

BACKGROUND
Myocardial fibrosis may increase vulnerability to poor prognosis in patients with heart failure (HF), even in those patients exhibiting left ventricular reverse remodeling (LVRR) after guideline-based therapies.
OBJECTIVES
This study sought to characterize fibrosis at baseline in patients with HF with left ventricular ejection fraction (LVEF) <50% by determining serum collagen type I-derived peptides (procollagen type I C-terminal propeptide [PICP] and ratio of collagen type I C-terminal telopeptide to matrix metalloproteinase-1) and to evaluate their association with LVRR and prognosis.
METHODS
Peptides were determined in 1,034 patients with HF at baseline. One-year echocardiography was available in 665 patients. Associations of peptides with 1-year changes in echocardiographic variables were analyzed by multivariable linear mixed models. LVEF was considered improved if it increased by ≥15% or to ≥50% or if it increased by ≥10% to >40% in patients with LVEF ≤40%. Cardiovascular death and HF-related outcomes were analyzed in all patients randomized to derivation (n = 648) and validation (n = 386) cohorts.
RESULTS
Continuous associations with echocardiographic changes were observed only for PICP. Compared with high-PICP (≥108.1 ng/mL) patients, low-PICP (<108.1 ng/mL) patients exhibited enhanced LVRR and a lower risk of HF-related outcomes (P ≤ 0.018), with women and nonischemic patients with HF showing a stronger LVEF increase (interaction P ≤ 0.010). LVEF increase was associated with a better prognosis, particularly in low-PICP patients (interaction P ≤ 0.029). Only patients with both low PICP and improved LVEF exhibited a better clinical evolution than patients with nonimproved LVEF (P < 0.001).
CONCLUSIONS
Phenotyping with PICP, a peptide associated with myocardial fibrosis, may be useful to differentiate patients with HF who are more likely to experience clinical myocardial recovery from those with partial myocardial improvement.

Identifiants

pubmed: 36599551
pii: S2213-1779(22)00576-5
doi: 10.1016/j.jchf.2022.09.008
pii:
doi:

Substances chimiques

Procollagen Type I 0
Collagen Type I 0
Peptide Fragments 0
Procollagen 0
Biomarkers 0
Collagen 9007-34-5
Peptides 0

Types de publication

Randomized Controlled Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

58-72

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2023 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Funding Support and Author Disclosures This work was supported by grants from the Spanish Ministry of Science, Innovation, and Universities (MICINN) (SAF2017-84324-C2-1-R, SAF2017-85574-R and DPI2017-83721-P); the Institute of Health Carlos III (ISCIII) (PI17/01487, PI18/00256, PIC18/00014, PI18/01469 and PI20/01319), CIBER Cardiovascular (CB16/11/00403 and CB16/11/00483) projects, as a part of the National R&D&I Plan, cofunded by ISCIII-Sub-Directorate-General for Research Assessment and Promotion and the European Regional Development Fund (ERDF); Directorate General of Industry, Energy and Innovation, Government of Navarra (MINERVA II project) and the European Commission (HOMAGE-2012-305507 and H2020-CRUCIAL-2019-848109-2). Dr Bayés-Genís has received grants and personal fees from AstraZeneca, Vifor, Boehringer Ingelheim, Novartis, Roche Diagnostics, and Critical diagnostics. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Susana Ravassa (S)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain. Electronic address: sravassa@unav.es.

Josep Lupón (J)

Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain; Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain.

Begoña López (B)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain.

Pau Codina (P)

Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain.

Mar Domingo (M)

Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain.

Elena Revuelta-López (E)

Heart Failure and Cardiac Regeneration (ICREC) Research Program, Germans Trias i Pujol Health Science Research Institute, Badalona, Spain.

María U Moreno (MU)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain.

Gorka San José (G)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain.

Evelyn Santiago-Vacas (E)

Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain.

Germán Cediel (G)

Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain.

Carmen Roncal (C)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain.

Javier Díez (J)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain.

Antoni Bayés-Genís (A)

Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain; Cardiology Service and Cardiac Insufficiency Unit, Germans Trias i Pujol University Hospital, Badalona, Spain; Department of Medicine, Autonomous University of Barcelona, Barcelona, Spain; Heart Failure and Cardiac Regeneration (ICREC) Research Program, Germans Trias i Pujol Health Science Research Institute, Badalona, Spain.

Arantxa González (A)

Program of Cardiovascular Diseases, Center for Applied Medical Research (CIMA), University of Navarra, Pamplona, Spain; Navarra Institute for Health Research (IdiSNA), Pamplona, Spain; Network Center for Biomedical Research into Cardiovascular Diseases (CIBERCV), Carlos III Institute of Health, Madrid, Spain. Electronic address: amiqueo@unav.es.

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Classifications MeSH