Cytokine Networks and Heart Failure Outcomes

Inflammation and congestion constitute fundamental mechanisms underlying heart failure (HF). Carbohydrate Antigen 125 (CA125) is a well-established biomarker in HF, primarily associated with congestion, but also it may act as a functional ligand amplifying the inflammatory response in HF. Our aim wa...

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Detalles Bibliográficos
Autores: Santas, Enrique, Martí-Martínez, Arancha, Villar, Sandra|||0000-0001-8229-6279, De la Espriella, Rafael|||0000-0002-8720-3999, Rodriguez-Borja, Enrique|||0000-0002-0339-6704, Revuelta-López, Elena|||0000-0001-8962-5936, González, Arantxa|||0000-0001-5986-6528, Bayés-Genís, Antoni|||0000-0002-3044-197X, Sanchis, Juan|||0000-0003-0797-8709, Núñez, Julio|||0000-0003-1672-7119
Tipo de recurso: artículo
Fecha de publicación:2025
País:España
Institución:Universitat Autònoma de Barcelona
Repositorio:Dipòsit Digital de Documents de la UAB
Idioma:inglés
OAI Identifier:oai:dnet:uabarcelona_::6ce120d6c281d0ad67d95540fa6de9f7
Acceso en línea:https://ddd.uab.cat/record/327785
https://dx.doi.org/urn:doi:10.3390/ijms26199527
Access Level:acceso abierto
Palabra clave:Heart failure
Inflammation
Antigen carbohydrate 125
Cytokines
Descripción
Sumario:Inflammation and congestion constitute fundamental mechanisms underlying heart failure (HF). Carbohydrate Antigen 125 (CA125) is a well-established biomarker in HF, primarily associated with congestion, but also it may act as a functional ligand amplifying the inflammatory response in HF. Our aim was to evaluate the potential modulatory effect of CA125 on inflammation, assessed by a set of cytokines (interleukin [IL]-6, IL-10, IL-1β, and tumor necrosis factor [TNF]). We prospectively included 284 patients admitted for acute HF in which cytokines and CA125 were assessed at admission. Study endpoints were all-cause mortality and total HF rehospitalizations. At a median follow-up of 4.2 years (interquartile range: 1.3-7.5), a total of 211 patients (74.3%) died, and 117 patients (41.2%) experienced 249 HF readmissions. In the multivariable analysis, a significant interaction between IL-6 and IL-10 and CA125 was observed for both outcomes (p -value for interactions < 0.05 for all comparisons). Among patients with CA125 > 35 U/mL, both IL-6 and IL-10 showed a positive, linear relationship with the risk of death or HF readmissions. In contrast, we did not find a significant association in patients with CA125 ≤ 35 U/mL. In conclusion, the association between IL-6 and IL-10 with long-term adverse events was significantly modulated by CA125 status, being significantly associated with poor prognosis only when CA125 was upregulated. These findings support a potential modulatory role for CA125 in the inflammatory response in HF.