Inflammatory markers in Eisenmenger syndrome and their association with clinical outcomes. A cross-sectional comparative study.
Congenital heart disease
Eisenmenger syndrome
Inflammation
Pulmonary circulation
Pulmonary hypertension
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 Nov 2021
01 Nov 2021
Historique:
received:
15
01
2021
revised:
02
04
2021
accepted:
18
06
2021
pubmed:
26
6
2021
medline:
21
10
2021
entrez:
25
6
2021
Statut:
ppublish
Résumé
Inflammation may be an important factor contributing to the progression of Eisenmenger syndrome (ES). The purpose of the current study was to: characterize the inflammatory profile in ES patients and compare measures to reference values for congenital heart disease and pulmonary arterial hypertension (CHD-PAH); and investigate whether inflammatory markers are associated with other clinical markers in ES. Twenty-seven ES patients were prospectively selected and screened for systemic inflammatory markers, including interleukin (IL)-1β, tumor necrosis factor-alpha (TNF-α) and IL-10. Clinical data and echocardiographic parameters were obtained, with concomitant analysis of ventricular function. Functional capacity was assessed using the 6-min walk test (6MWT). Renal function and blood homeostasis were evaluated by the level of blood urea nitrogen (BUN), creatinine, and plasma electrolytes. Patients with ES expressed higher IL-10, IL-1β and TNF-α compared to reference values of patients with CHD-PAH. IL-10 was negatively associated with BUN (r = -0.39,p = 0.07), creatinine (r = -0.35, p = 0.002), sodium (r = -0.45, p = 0.03), and potassium (r = -0.68, p = 0.003). IL-10 was positively associated with bicarbonate (r = 0.45, p = 0.02) and trended toward a positive association with right ventricular fractional area change (RV ES patients exhibit a more severe inflammatory profile compared to reference values for CHD-PAH. Furthermore, inflammatory markers are related to renal dysfunction, right ventricular impairment and poorer functional capacity.
Sections du résumé
BACKGROUND
BACKGROUND
Inflammation may be an important factor contributing to the progression of Eisenmenger syndrome (ES). The purpose of the current study was to: characterize the inflammatory profile in ES patients and compare measures to reference values for congenital heart disease and pulmonary arterial hypertension (CHD-PAH); and investigate whether inflammatory markers are associated with other clinical markers in ES.
METHODS
METHODS
Twenty-seven ES patients were prospectively selected and screened for systemic inflammatory markers, including interleukin (IL)-1β, tumor necrosis factor-alpha (TNF-α) and IL-10. Clinical data and echocardiographic parameters were obtained, with concomitant analysis of ventricular function. Functional capacity was assessed using the 6-min walk test (6MWT). Renal function and blood homeostasis were evaluated by the level of blood urea nitrogen (BUN), creatinine, and plasma electrolytes.
RESULTS
RESULTS
Patients with ES expressed higher IL-10, IL-1β and TNF-α compared to reference values of patients with CHD-PAH. IL-10 was negatively associated with BUN (r = -0.39,p = 0.07), creatinine (r = -0.35, p = 0.002), sodium (r = -0.45, p = 0.03), and potassium (r = -0.68, p = 0.003). IL-10 was positively associated with bicarbonate (r = 0.45, p = 0.02) and trended toward a positive association with right ventricular fractional area change (RV
CONCLUSION
CONCLUSIONS
ES patients exhibit a more severe inflammatory profile compared to reference values for CHD-PAH. Furthermore, inflammatory markers are related to renal dysfunction, right ventricular impairment and poorer functional capacity.
Identifiants
pubmed: 34171450
pii: S0167-5273(21)01037-8
doi: 10.1016/j.ijcard.2021.06.039
pii:
doi:
Substances chimiques
Biomarkers
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
34-38Informations de copyright
Copyright © 2021. Published by Elsevier B.V.