Assessment of TNF-α expression in unstable atherosclerotic plaques, serum IL-6 and TNF-α levels in patients with acute coronary syndrome and rheumatoid arthritis.
Coronary syndrome
High-sensitivity C-reactive protein
Interleukin-6
Rheumatoid arthritis
Tumor necrosis factor-alpha
Journal
Rheumatology international
ISSN: 1437-160X
Titre abrégé: Rheumatol Int
Pays: Germany
ID NLM: 8206885
Informations de publication
Date de publication:
09 2022
09 2022
Historique:
received:
24
01
2022
accepted:
07
03
2022
pubmed:
26
5
2022
medline:
6
8
2022
entrez:
25
5
2022
Statut:
ppublish
Résumé
The role of inflammatory cytokines is well researched in acute coronary syndrome (ACS) and rheumatoid arthritis (RA), but not in the presence of both conditions. This study aimed to compare TNF-α expression, serum TNF-α, IL-6, and hs-CRP in ACS patients with RA (n = 46) with ACS patients without RA (n = 49) and healthy controls (n = 50). TNF-α expression was assessed from coronary artery samples, taken during coronary artery bypass surgery. Serum levels TNF-α, IL-6, and hs-CRP were measured 24 and 48 h after cardiac surgery. Stronger TNF-α expression was observed in the ACS patients with RA versus the ACS patients without RA, p = 0.001. Serum TNF-α, IL-6, and hs-CRP at the 24th h were significantly elevated in both patient groups and distinguished them from the healthy controls with accuracy ranging from 80 to 99%. At the 48th h, serum TNF-α and IL-6 in the ACS group without RA decreased to those of the healthy controls but remained high in the group with RA. ACS cases with RA could be correctly identified from the levels of IL-6 (AUC = 0.885, 95% CI 0.791 to 0.938) and TNF-α (AUC = 0.852, 95%CI 0.720 to 0.922). Our results suggest that the presence of RA in ACS cases is likely to provoke stronger TNF-α expression on atherosclerotic plaques, aggravate the pro-inflammatory response, and sustain it even after the cardiac stress is lowered. In ACS cases with RA, long-term monitoring and control of TNF-α and IL-6 levels can be a useful preventive strategy.
Identifiants
pubmed: 35614271
doi: 10.1007/s00296-022-05113-4
pii: 10.1007/s00296-022-05113-4
doi:
Substances chimiques
Biomarkers
0
Interleukin-6
0
Tumor Necrosis Factor-alpha
0
C-Reactive Protein
9007-41-4
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1589-1596Informations de copyright
© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.
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