Clinical and Humoral Determinants of Congestion in Heart Failure: Potential Role of Adiponectin.


Journal

Kidney & blood pressure research
ISSN: 1423-0143
Titre abrégé: Kidney Blood Press Res
Pays: Switzerland
ID NLM: 9610505

Informations de publication

Date de publication:
2019
Historique:
received: 22 03 2019
accepted: 28 08 2019
pubmed: 26 9 2019
medline: 4 3 2020
entrez: 26 9 2019
Statut: ppublish

Résumé

Some patients with heart failure (HF) are more prone to systemic congestion than others. The goal of this study was to identify clinical and humoral factors linked to congestion and its prognostic impact in HF patients. A total of 371 advanced HF patients underwent physical examination, echocardiography, right heart catheterization, blood samplings, and Minnesota Living with HF Questionnaire. Subjects were followed-up for adverse events (death, urgent transplantation, or assist device implantation without heart transplantation). Thirty-one percent of patients were classified as prone to congestion. During a median follow-up of 1,093 days, 159 (43%) patients had an adverse event. In the Cox analysis, the congestion-prone (CP) status was associated with a 43% higher event risk. The CP status was strongly (p ˂ 0.001) associated with body weight loss, right ventricular dysfunction (RVD), dilated inferior vena cava (IVC), diuretics, and beta-blockers prescription and the majority of tested hormones in the univariate analysis. In the multivariate analysis, the only independent variables associated with the CP status were adiponectin, albumin, IVC diameter, and RVD. Adiponectin by itself was predictive of adverse events. In a multivariate model, CP status was no longer predictive of adverse events, in contrast to adiponectin. CP patients experienced more severe symptoms and had shorter survival. Potential role of adiponectin, a new independent predictor of CP status, should be further examined.

Sections du résumé

BACKGROUND BACKGROUND
Some patients with heart failure (HF) are more prone to systemic congestion than others. The goal of this study was to identify clinical and humoral factors linked to congestion and its prognostic impact in HF patients.
METHODS METHODS
A total of 371 advanced HF patients underwent physical examination, echocardiography, right heart catheterization, blood samplings, and Minnesota Living with HF Questionnaire. Subjects were followed-up for adverse events (death, urgent transplantation, or assist device implantation without heart transplantation).
RESULTS RESULTS
Thirty-one percent of patients were classified as prone to congestion. During a median follow-up of 1,093 days, 159 (43%) patients had an adverse event. In the Cox analysis, the congestion-prone (CP) status was associated with a 43% higher event risk. The CP status was strongly (p ˂ 0.001) associated with body weight loss, right ventricular dysfunction (RVD), dilated inferior vena cava (IVC), diuretics, and beta-blockers prescription and the majority of tested hormones in the univariate analysis. In the multivariate analysis, the only independent variables associated with the CP status were adiponectin, albumin, IVC diameter, and RVD. Adiponectin by itself was predictive of adverse events. In a multivariate model, CP status was no longer predictive of adverse events, in contrast to adiponectin.
CONCLUSIONS CONCLUSIONS
CP patients experienced more severe symptoms and had shorter survival. Potential role of adiponectin, a new independent predictor of CP status, should be further examined.

Identifiants

pubmed: 31553971
pii: 000502975
doi: 10.1159/000502975
doi:

Substances chimiques

Adiponectin 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1271-1284

Informations de copyright

© 2019 The Author(s) Published by S. Karger AG, Basel.

Auteurs

Luca Monzo (L)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia, luca.monzo@uniroma1.it.
Department of Cardiovascular, Respiratory, Nephrological, Anaesthetic and Geriatric Sciences, "Sapienza" University, Rome, Italy, luca.monzo@uniroma1.it.

Martin Kotrc (M)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Jan Benes (J)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Kamil Sedlacek (K)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Ivana Jurcova (I)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Janka Franekova (J)

Department of Laboratory Methods, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Petr Jarolim (P)

Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.

Josef Kautzner (J)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

Vojtech Melenovsky (V)

Department of Cardiology, Institute of Clinical and Experimental Medicine, Prague, Czechia.

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