Cardiovascular Risk in Patients With Takayasu Arteritis Directly Correlates With Diastolic Dysfunction and Inflammatory Cell Infiltration in the Vessel Wall: A Clinical,
Regulatory T Lymphocytes (Tregs)
T helper-like cells
Takayasu arteritis (TAK)
echocardiography
immune cell infiltration
vascular stiffness
Journal
Frontiers in medicine
ISSN: 2296-858X
Titre abrégé: Front Med (Lausanne)
Pays: Switzerland
ID NLM: 101648047
Informations de publication
Date de publication:
2022
2022
Historique:
received:
26
01
2022
accepted:
11
04
2022
entrez:
2
6
2022
pubmed:
3
6
2022
medline:
3
6
2022
Statut:
epublish
Résumé
Takayasu Arteritis (TAK) increases vascular stiffness and arterial resistance. Atherosclerosis leads to similar changes. We investigated possible differences in cardiovascular remodeling between these diseases and whether the differences are correlated with immune cell expression. Patients with active TAK arteritis were compared with age- and sex-matched atherosclerotic patients (Controls). In a subpopulation of TAK patients, Treg/Th17 cells were measured before (T0) and after 18 months (T18) of infliximab treatment. Echocardiogram, supraaortic Doppler ultrasound, and lymphocytogram were performed in all patients. Histological and immunohistochemical changes of the vessel wall were evaluated as well. TAK patients have increased aortic valve dysfunction and diastolic dysfunction. The degree of dysfunction appears associated with uric acid levels. A significant increase in aortic stiffness was also observed and associated with levels of peripheral T lymphocytes. CD3 Our data suggest that different pathogenic mechanisms underlie vessel damage, including atherosclerosis, in TAK patients compared with Controls. The increased risk of ASCVD in TAK patients correlates directly with the degree of inflammatory cell infiltration in the vessel wall. Infliximab restores the normal frequency of Tregs/Th17 in TAK patients and allows a possible reduction of steroids and immunosuppressants.
Sections du résumé
Background
UNASSIGNED
Takayasu Arteritis (TAK) increases vascular stiffness and arterial resistance. Atherosclerosis leads to similar changes. We investigated possible differences in cardiovascular remodeling between these diseases and whether the differences are correlated with immune cell expression.
Methods
UNASSIGNED
Patients with active TAK arteritis were compared with age- and sex-matched atherosclerotic patients (Controls). In a subpopulation of TAK patients, Treg/Th17 cells were measured before (T0) and after 18 months (T18) of infliximab treatment. Echocardiogram, supraaortic Doppler ultrasound, and lymphocytogram were performed in all patients. Histological and immunohistochemical changes of the vessel wall were evaluated as well.
Results
UNASSIGNED
TAK patients have increased aortic valve dysfunction and diastolic dysfunction. The degree of dysfunction appears associated with uric acid levels. A significant increase in aortic stiffness was also observed and associated with levels of peripheral T lymphocytes. CD3
Conclusion
UNASSIGNED
Our data suggest that different pathogenic mechanisms underlie vessel damage, including atherosclerosis, in TAK patients compared with Controls. The increased risk of ASCVD in TAK patients correlates directly with the degree of inflammatory cell infiltration in the vessel wall. Infliximab restores the normal frequency of Tregs/Th17 in TAK patients and allows a possible reduction of steroids and immunosuppressants.
Identifiants
pubmed: 35652080
doi: 10.3389/fmed.2022.863150
pmc: PMC9149422
doi:
Types de publication
Journal Article
Langues
eng
Pagination
863150Informations de copyright
Copyright © 2022 Cicco, Desantis, Vacca, Cazzato, Solimando, Cirulli, Noviello, Susca, Prete, Brosolo, Catena, Lamanuzzi, Saltarella, Frassanito, Cimmino, Ingravallo, Resta, Ria and Montagnani.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
FASEB J. 2014 Jul;28(7):3197-204
pubmed: 24652948
J Hypertens. 2008 Feb;26(2):269-75
pubmed: 18192841
Hypertension. 2015 May;65(5):1015-9
pubmed: 25776078
Arthritis Rheum. 2005 Feb 15;53(1):100-7
pubmed: 15696576
Br J Rheumatol. 1993 Aug;32(8):666-70
pubmed: 8348267
Medicine (Baltimore). 2020 Sep 25;99(39):e22406
pubmed: 32991468
Clin Exp Immunol. 2008 May;152(2):311-9
pubmed: 18341609
Rheumatology (Oxford). 2012 May;51(5):882-6
pubmed: 22223706
Nat Immunol. 2018 Jul;19(7):665-673
pubmed: 29925983
Semin Arthritis Rheum. 2021 Aug;51(4):911-918
pubmed: 33272608
Arch Med Sci. 2013 Apr 20;9(2):268-75
pubmed: 23671437
Am J Cardiol. 2019 Sep 1;124(5):723-728
pubmed: 31266594
Mediators Inflamm. 2020 Jul 16;2020:7527953
pubmed: 32724296
J Am Soc Nephrol. 2005 Dec;16(12):3553-62
pubmed: 16251237
Eur Heart J. 1990 Nov;11(11):990-6
pubmed: 2282929
Clin Exp Med. 2020 Feb;20(1):11-19
pubmed: 31848778
Eur Heart J. 2018 Mar 1;39(9):763-816
pubmed: 28886620
Life (Basel). 2020 Oct 18;10(10):
pubmed: 33081052
Nutr Metab Cardiovasc Dis. 2022 Feb;32(2):420-428
pubmed: 34893418
Int J Environ Res Public Health. 2013 Aug 27;10(9):3834-42
pubmed: 23985769
Clin Exp Immunol. 2009 Jun;156(3):395-404
pubmed: 19309348
J Cell Biol. 2007 Oct 8;179(1):33-40
pubmed: 17923528
Circ Res. 2007 Feb 2;100(2):204-12
pubmed: 17218606
Curr Rheumatol Rep. 2020 Nov 7;22(12):88
pubmed: 33159612
Int Rev Immunol. 2012 Dec;31(6):462-73
pubmed: 23215768
Curr Rheumatol Rep. 2020 Oct 12;22(12):84
pubmed: 33044642
Arthritis Care Res (Hoboken). 2020 Nov;72(11):1615-1624
pubmed: 31444857
Am J Physiol Cell Physiol. 2008 Nov;295(5):C1183-90
pubmed: 18784379
Hypertension. 2015 Jun;65(6):1231-7
pubmed: 25801873
Oman Med J. 2021 May 31;36(3):e262
pubmed: 34164156
Clin Exp Rheumatol. 2020 Mar-Apr;38 Suppl 124(2):48-54
pubmed: 31969221
S Afr Med J. 2014 Aug 20;104(10):671-4
pubmed: 25363050
Trials. 2007 Nov 26;8:38
pubmed: 18039364
J Hum Hypertens. 2022 Jul;36(7):651-658
pubmed: 34117347
Curr Probl Cardiol. 2021 May;46(5):100819
pubmed: 33631706
Ochsner J. 2009 Winter;9(4):191-6
pubmed: 21603443
Nitric Oxide. 2007 Mar;16(2):266-73
pubmed: 17166753
Heart Vessels. 2008 May;23(3):209-13
pubmed: 18484166
Hypertension. 2018 Jan;71(1):78-86
pubmed: 29203632
Arthritis Res Ther. 2020 Jun 5;22(1):131
pubmed: 32503678
Ann Rheum Dis. 2020 Jan;79(1):19-30
pubmed: 31270110
Yonsei Med J. 2012 Mar;53(2):258-61
pubmed: 22318811
Int J Cardiol. 2018 Jun 15;261:183-188
pubmed: 29551256
Eur Heart J. 2018 Sep 1;39(33):3021-3104
pubmed: 30165516
Curr Probl Cardiol. 2021 May 29;:100900
pubmed: 34167843
Lancet. 2008 Jul 19;372(9634):234-45
pubmed: 18640460
J Am Soc Echocardiogr. 2015 Jan;28(1):1-39.e14
pubmed: 25559473
Stroke. 1999 Sep;30(9):1751-8
pubmed: 10471419
Blood. 1997 Jan 15;89(2):577-82
pubmed: 9002961
J Am Coll Cardiol. 2020 Oct 6;76(14):1660-1670
pubmed: 33004131
Arthritis Rheumatol. 2021 Aug;73(8):1349-1365
pubmed: 34235884
Vascul Pharmacol. 2018 Jan;100:1-19
pubmed: 28579545
N Engl J Med. 2003 Jul 10;349(2):160-9
pubmed: 12853590
Immunol Rev. 2007 Dec;220:35-46
pubmed: 17979838
Front Biosci (Landmark Ed). 2012 Jan 01;17(2):656-69
pubmed: 22201767
Vasc Cell. 2015 Sep 18;7:8
pubmed: 26388991
J Am Coll Cardiol. 2017 Mar 28;69(12):1617-1636
pubmed: 27825770
Curr Vasc Pharmacol. 2019;17(1):99-106
pubmed: 29278214
Eur J Clin Invest. 2014 Oct;44(10):972-81
pubmed: 25186106
Circulation. 2002 Mar 12;105(10):1202-7
pubmed: 11889014
Rheum Dis Clin North Am. 1995 Feb;21(1):73-80
pubmed: 7732175
Signal Transduct Target Ther. 2017;2:
pubmed: 29158945
Clin Chem. 2020 Nov 1;66(11):1434-1443
pubmed: 33276383
J Cardiol. 2021 Jul;78(1):51-57
pubmed: 33388217
J Immunother Cancer. 2021 Jun;9(6):
pubmed: 34168005
Biochem Pharmacol. 2009 Sep 15;78(6):539-52
pubmed: 19413999
J Lipid Res. 2003 Mar;44(3):512-21
pubmed: 12562831
Ann Dermatol Venereol. 2019 Jun - Jul;146(6-7):483-486
pubmed: 31230775