Metabolic changes contribute to maladaptive right ventricular hypertrophy in pulmonary hypertension beyond pressure overload: an integrative imaging and omics investigation.

Cardiac imaging Omics Pulmonary hypertension Right ventricle

Journal

Basic research in cardiology
ISSN: 1435-1803
Titre abrégé: Basic Res Cardiol
Pays: Germany
ID NLM: 0360342

Informations de publication

Date de publication:
27 Mar 2024
Historique:
received: 09 11 2023
accepted: 10 02 2024
revised: 10 02 2024
medline: 27 3 2024
pubmed: 27 3 2024
entrez: 27 3 2024
Statut: aheadofprint

Résumé

Right ventricular (RV) failure remains the strongest determinant of survival in pulmonary hypertension (PH). We aimed to identify relevant mechanisms, beyond pressure overload, associated with maladaptive RV hypertrophy in PH. To separate the effect of pressure overload from other potential mechanisms, we developed in pigs two experimental models of PH (M1, by pulmonary vein banding and M2, by aorto-pulmonary shunting) and compared them with a model of pure pressure overload (M3, pulmonary artery banding) and a sham-operated group. Animals were assessed at 1 and 8 months by right heart catheterization, cardiac magnetic resonance and blood sampling, and myocardial tissue was analyzed. Plasma unbiased proteomic and metabolomic data were compared among groups and integrated by an interaction network analysis. A total of 33 pigs completed follow-up (M1, n = 8; M2, n = 6; M3, n = 10; and M0, n = 9). M1 and M2 animals developed PH and reduced RV systolic function, whereas animals in M3 showed increased RV systolic pressure but maintained normal function. Significant plasma arginine and histidine deficiency and complement system activation were observed in both PH models (M1&M2), with additional alterations to taurine and purine pathways in M2. Changes in lipid metabolism were very remarkable, particularly the elevation of free fatty acids in M2. In the integrative analysis, arginine-histidine-purines deficiency, complement activation, and fatty acid accumulation were significantly associated with maladaptive RV hypertrophy. Our study integrating imaging and omics in large-animal experimental models demonstrates that, beyond pressure overload, metabolic alterations play a relevant role in RV dysfunction in PH.

Identifiants

pubmed: 38536505
doi: 10.1007/s00395-024-01041-5
pii: 10.1007/s00395-024-01041-5
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Instituto de Salud Carlos III
ID : PI17/00995
Organisme : Instituto de Salud Carlos III
ID : PI20/00742
Organisme : Ministerio de Ciencia, Innovación y Universidades
ID : PID2021-122348NB-I00
Organisme : Ministerio de Ciencia, Innovación y Universidades
ID : PLEC2022-009235
Organisme : Ministerio de Ciencia, Innovación y Universidades
ID : PLEC2022-009298
Organisme : Comunidad de Madrid
ID : IMMUNO-VAR
Organisme : Comunidad de Madrid
ID : P2022/BMD-7333
Organisme : 'la Caixa' Foundation
ID : HR17-00247
Organisme : 'la Caixa' Foundation
ID : HR22-00253

Informations de copyright

© 2024. The Author(s).

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Auteurs

Inés García-Lunar (I)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Cardiology Department, University Hospital La Moraleja, Madrid, Spain.

Inmaculada Jorge (I)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.

Jorge Sáiz (J)

Centre of Metabolomics and Bioanalysis (CEMBIO), Department of Chemistry and Biochemistry, Facultad de Farmacia, Universidad San Pablo-CEU, Madrid, Spain.

Núria Solanes (N)

Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.

Ana Paula Dantas (AP)

Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.

Juan José Rodríguez-Arias (JJ)

Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.

María Ascaso (M)

Department of Cardiovascular Surgery, Hospital Clínic Barcelona, Barcelona, Spain.

Carlos Galán-Arriola (C)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.

Francisco Rafael Jiménez (FR)

Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.

Elena Sandoval (E)

Department of Cardiovascular Surgery, Hospital Clínic Barcelona, Barcelona, Spain.

Jorge Nuche (J)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Department of Cardiology, Hospital 12 de Octubre, Madrid, Spain.

Maria Moran-Garrido (M)

Centre of Metabolomics and Bioanalysis (CEMBIO), Department of Chemistry and Biochemistry, Facultad de Farmacia, Universidad San Pablo-CEU, Madrid, Spain.

Emilio Camafeita (E)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.

Montserrat Rigol (M)

Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain.

Javier Sánchez-Gonzalez (J)

Philips Healthcare Iberia, Madrid, Spain.

Valentín Fuster (V)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
Mount Sinai Fuster Heart Hospital, Mount Sinai Hospital, New York, NY, USA.

Jesús Vázquez (J)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.

Coral Barbas (C)

Centre of Metabolomics and Bioanalysis (CEMBIO), Department of Chemistry and Biochemistry, Facultad de Farmacia, Universidad San Pablo-CEU, Madrid, Spain.

Borja Ibáñez (B)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
IIS-Fundación Jiménez Diaz University Hospital, Madrid, Spain.

Daniel Pereda (D)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Department of Cardiovascular Surgery, Hospital Clínic Barcelona, Barcelona, Spain.
Universitat de Barcelona, Barcelona, Spain.

Ana García-Álvarez (A)

Centro Nacional de Investigaciones Cardiovasculares Carlos III (CNIC), Madrid, Spain. anagarci@clinic.cat.
CIBER de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain. anagarci@clinic.cat.
Department of Cardiology, Hospital Clínic Barcelona-IDIBAPS, Universitat de Barcelona, Villarroel 170, 08036, Barcelona, Spain. anagarci@clinic.cat.
Universitat de Barcelona, Barcelona, Spain. anagarci@clinic.cat.

Classifications MeSH