Biomarker-associated Monocyte Inflammatory Signaling in Myocardial Infarction

Imagem de Miniatura
Arquivos
art_GUIMARÃES_Biomarkerassociated_Monocyte_Inflammatory_Signaling_in_Myocardial_Infarction_2023.PDF (686.93 KB)
Citações na Scopus
1
Tipo de produção
article
Data de publicação
2023
DOI
SciELO
Scopus
Título da Revista
ISSN da Revista
Título do Volume
Editora
Sociedade Brasileira de Cardiologia
Autores
GUIMARÃES, Raphael Boesche
LEITE, Rogério Sarmento
DUTRA, Oscar
CASTRO, Iran
MANICA, André Luiz
Citação
INTERNATIONAL JOURNAL OF CARDIOVASCULAR SCIENCES, v.36, p.e20220007, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Abstract Background: Monocytes are essential components in inflammatory signaling, and their recruitment is crucial in the signaling pathway, which directs and determines cell adhesion to the activated endothelium. A better understanding of the correlation between monocyte subsets and inflammatory signaling in patients with atherosclerotic disease in acute coronary syndrome (ACS) is essential for the development of more effective therapies for the prevention and treatment of cardiovascular diseases. Objective: To analyze differences between biomarkers and monocyte activation in the setting of ischemic heart disease. Methods: This was a case-control study comparing biomarkers and monocyte subsets between patients with ACS with and without ST-segment elevation and individuals without coronary stenosis. The nonparametric Kruskal-Wallis test was used to assess differences between groups, and Dunn's post hoc test was used to identify which groups were different. Cuzick's test for ordered group trends was used to assess falling or rising trends. Participants were classified into 3 groups: control (0); non-ST-elevation myocardial infarction (NSTEMI) (1); ST-elevation myocardial infarction (STEMI) D1 (2). Results: Forty-seven patients with ACS and 19 controls with no obstructive lesions on coronary angiography were recruited. Monocyte profile assessment was statistically different regarding time of symptom onset and the presence or absence of atherosclerotic disease (Kruskal-Wallis, p = 0.0009). Dunn's post hoc test showed a significant difference between the control group and the STEMI D1 (p = 0.0014), STEMI D3 (p = 0.0036), and STEMI D7 (p = 0.0195) groups, corresponding to a 2-fold increase in classical (p = 0.0022) and nonclassical (p = 0.0031) monocytes compared with controls. For classical monocytes, there was a difference between the control group and all STEMI groups and between the NSTEMI group and the STEMI D1, D3, and D7 groups. For nonclassical monocytes, there was a difference between the control group and the STEMI D7 group (p = 0.0056) and between the NSTEMI group and the STEMI D7 group (p = 0.0166). Conclusion: This study found that there was an increase in total and classical monocyte mobilization at the time of acute myocardial infarction in patients with ACS.
Palavras-chave
Myocardial infarction, Monocytes, Atherosclerosis
URI
https://observatorio.fm.usp.br/handle/OPI/53352
Referências
  1. Afiune Neto Abrahão, 2006, Arq. Bras. Cardiol., V86, P240, DOI 10.1590/S0066-782X2006000300013
  2. [Anonymous], 2017, Circulation, V136, pe196, DOI 10.1161/CIR.0000000000000530
  3. Cetin EHO, 2015, BIOMARK MED, V9, P967, DOI 10.2217/bmm.15.74
  4. CUZICK J, 1985, STAT MED, V4, P87, DOI 10.1002/sim.4780040112
  5. Dinarello CA, 2009, ANNU REV IMMUNOL, V27, P519, DOI 10.1146/annurev.immunol.021908.132612
  6. Gistera A, 2017, NAT REV NEPHROL, V13, DOI 10.1038/nrneph.2017.51
  7. Hansson GK, 2015, J INTERN MED, V278, P483, DOI 10.1111/joim.12406
  8. Imanishi T, 2010, ATHEROSCLEROSIS, V212, P628, DOI 10.1016/j.atherosclerosis.2010.06.025
  9. Italiani P, 2014, FRONT IMMUNOL, V5, DOI 10.3389/fimmu.2014.00514
  10. Jain MK, 2014, ARTERIOSCL THROM VAS, V34, P499, DOI 10.1161/ATVBAHA.113.301925
  11. Kashiwagi M, 2010, ATHEROSCLEROSIS, V212, P171, DOI 10.1016/j.atherosclerosis.2010.05.004
  12. Ketelhuth DFJ, 2016, CIRC RES, V118, P668, DOI 10.1161/CIRCRESAHA.115.306427
  13. Libby P, 2015, CIRC RES, V116, P307, DOI 10.1161/CIRCRESAHA.116.301313
  14. Libby P, 2009, J AM COLL CARDIOL, V54, P2129, DOI 10.1016/j.jacc.2009.09.009
  15. Lichtman AH, 2013, J CLIN INVEST, V123, P27, DOI 10.1172/JCI63108
  16. Nus M, 2016, EXPERT REV CLIN IMMU, V12, P1217, DOI 10.1080/1744666X.2016.1195686
  17. Ridker PM, 2016, J AM COLL CARDIOL, V67, P712, DOI 10.1016/j.jacc.2015.11.037
  18. Ridker PM, 2005, NEW ENGL J MED, V352, P20, DOI 10.1056/NEJMoa042378
  19. Schlitt A, 2004, THROMB HAEMOSTASIS, V92, P419, DOI 10.1160/TH04-02-0095
  20. Schonbeck U, 2004, CIRCULATION, V109, P18, DOI 10.1161/01.CIR.0000129505.34151.23
  21. Swirski FK, 2007, J CLIN INVEST, V117, P195, DOI 10.1172/JCI29950
  22. Tardif JC, 2019, NEW ENGL J MED, V381, P2497, DOI 10.1056/NEJMoa1912388
  23. Thygesen K, 2018, EUR HEART J, V39, P3757, DOI 10.1093/eurheartj/ehy655
  24. Tsujioka H, 2009, J AM COLL CARDIOL, V54, P130, DOI 10.1016/j.jacc.2009.04.021
  25. Weber C, 2016, THROMB HAEMOSTASIS, V116, P626, DOI 10.1160/TH16-02-0091
  26. Woollard KJ, 2010, NAT REV CARDIOL, V7, P77, DOI 10.1038/nrcardio.2009.228
  27. ZIEGLERHEITBROCK HWL, 1993, EUR J IMMUNOL, V23, P2053, DOI 10.1002/eji.1830230902

Coleções
Artigos e Materiais de Revistas Científicas - HC/ICHC
Artigos e Materiais de Revistas Científicas - LIM/51
Artigos e Materiais de Revistas Científicas - ODS/03