Rheumatoid arthritis, as a clinical disease, but not rheumatoid arthritis-associated autoimmunity, is linked to cardiovascular events.
Anti-citrullinated protein autoantibody
Autoimmunity
Cardiovascular diseases
Cardiovascular risk
Rheumatoid arthritis
Journal
Arthritis research & therapy
ISSN: 1478-6362
Titre abrégé: Arthritis Res Ther
Pays: England
ID NLM: 101154438
Informations de publication
Date de publication:
24 02 2022
24 02 2022
Historique:
received:
26
07
2021
accepted:
13
01
2022
entrez:
25
2
2022
pubmed:
26
2
2022
medline:
11
3
2022
Statut:
epublish
Résumé
Rheumatoid arthritis (RA) is characterized by increased cardiovascular (CV) mortality. CV events are particularly high in patients with RA-specific autoimmunity, including rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA), raising the question whether RA-specific autoimmunity itself is associated with CV events. New CV events (myocardial infarction, stroke or death by CV cause) were recorded in 20,625 subjects of the Electricité de France - Gaz de France (GAZEL) cohort. Self-reported RA cases in the GAZEL cohort were validated by phone interview on the basis of a specific questionnaire. In 1618 subjects, in whom plasma was available, RF and ACPA were measured. A piecewise exponential Poisson regression was used to analyze the association of CV events with presence of RA as well as RA-specific autoimmunity (without RA). CV events in GAZEL were associated with age, male sex, smoking, hypertension, hyperlipidemia, and diabetes mellitus (HR from 1.06 to 1.87, p < 0.05). Forty-two confirmed RA cases were identified. Confirmed RA was significantly associated with CV risk increase (HR of 3.03; 95% CI: 1.13-8.11, p = 0.03) independently of conventional CV risk factors. One hundred seventy-eight subjects showed RF or ACPA positivity without presence of RA. CV events were not associated with ACPA positivity (HR: 1.52, 95% CI: 0.47-4.84, p = 0.48) or RF positivity (HR: 1.15, 95% CI: 0.55-2.40, p = 0.70) in the absence of RA. RA, as a clinical chronic inflammatory disease, but not mere positivity for RF or ACPA in the absence of clinical disease is associated with increased CV risk.
Sections du résumé
BACKGROUND
Rheumatoid arthritis (RA) is characterized by increased cardiovascular (CV) mortality. CV events are particularly high in patients with RA-specific autoimmunity, including rheumatoid factor (RF) and anti-citrullinated protein antibodies (ACPA), raising the question whether RA-specific autoimmunity itself is associated with CV events.
METHODS
New CV events (myocardial infarction, stroke or death by CV cause) were recorded in 20,625 subjects of the Electricité de France - Gaz de France (GAZEL) cohort. Self-reported RA cases in the GAZEL cohort were validated by phone interview on the basis of a specific questionnaire. In 1618 subjects, in whom plasma was available, RF and ACPA were measured. A piecewise exponential Poisson regression was used to analyze the association of CV events with presence of RA as well as RA-specific autoimmunity (without RA).
RESULTS
CV events in GAZEL were associated with age, male sex, smoking, hypertension, hyperlipidemia, and diabetes mellitus (HR from 1.06 to 1.87, p < 0.05). Forty-two confirmed RA cases were identified. Confirmed RA was significantly associated with CV risk increase (HR of 3.03; 95% CI: 1.13-8.11, p = 0.03) independently of conventional CV risk factors. One hundred seventy-eight subjects showed RF or ACPA positivity without presence of RA. CV events were not associated with ACPA positivity (HR: 1.52, 95% CI: 0.47-4.84, p = 0.48) or RF positivity (HR: 1.15, 95% CI: 0.55-2.40, p = 0.70) in the absence of RA.
CONCLUSIONS
RA, as a clinical chronic inflammatory disease, but not mere positivity for RF or ACPA in the absence of clinical disease is associated with increased CV risk.
Identifiants
pubmed: 35209936
doi: 10.1186/s13075-022-02722-z
pii: 10.1186/s13075-022-02722-z
pmc: PMC8867622
doi:
Substances chimiques
Anti-Citrullinated Protein Antibodies
0
Autoantibodies
0
Rheumatoid Factor
9009-79-4
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
56Informations de copyright
© 2022. The Author(s).
Références
Ann Rheum Dis. 2012 Sep;71(9):1524-9
pubmed: 22425941
Arthritis Res Ther. 2004;6(4):R303-8
pubmed: 15225365
Arterioscler Thromb Vasc Biol. 2014 Dec;34(12):2706-16
pubmed: 25256232
Arthritis Care Res (Hoboken). 2016 Jun;68(6):753-62
pubmed: 26473946
N Engl J Med. 2011 Dec 8;365(23):2205-19
pubmed: 22150039
J Clin Invest. 2012 May;122(5):1791-802
pubmed: 22505457
Arthritis Rheum. 2002 Aug;46(8):2010-9
pubmed: 12209502
Biometrics. 2016 Jun;72(2):546-53
pubmed: 26583951
Ann Rheum Dis. 2005 Oct;64(10):1427-30
pubmed: 15800010
J Cardiovasc Dis Res. 2013 Jun;4(2):102-6
pubmed: 24027365
Nat Immunol. 2017 Jan;18(1):104-113
pubmed: 27820809
Ann Rheum Dis. 2017 Jan;76(1):17-28
pubmed: 27697765
Arthritis Rheum. 2004 Mar;50(3):709-15
pubmed: 15022309
Int J Rheum Dis. 2017 Mar;20(3):287-297
pubmed: 28205331
Rheumatology (Oxford). 2013 Jan;52(1):68-75
pubmed: 23192907
Arthritis Care Res (Hoboken). 2020 Apr;72(4):561-576
pubmed: 30875456
Int J Epidemiol. 2007 Feb;36(1):32-9
pubmed: 17101614
Arthritis Rheum. 2004 Feb;50(2):380-6
pubmed: 14872479
Heart. 2020 Oct;106(20):1566-1572
pubmed: 32209618
Lancet. 2010 Jan 9;375(9709):132-40
pubmed: 20031199
PLoS One. 2016 Sep 06;11(9):e0162386
pubmed: 27598908
Am J Med. 2008 Oct;121(10 Suppl 1):S9-14
pubmed: 18926169
Int J Epidemiol. 2015 Feb;44(1):77-77g
pubmed: 25422284
Clin Exp Rheumatol. 2019 May-Jun;37(3):513
pubmed: 30789147
RMD Open. 2018 Nov 16;4(2):e000752
pubmed: 30564452
Arthritis Res Ther. 2007;9(6):R116
pubmed: 17986352
Rheumatol Int. 2017 Apr;37(4):487-493
pubmed: 28032180
Ann Rheum Dis. 2017 Oct;76(10):1693-1699
pubmed: 28606965
J Rheumatol. 1991 Sep;18(9):1282-4
pubmed: 1757925
J Rheumatol. 2009 Nov;36(11):2462-9
pubmed: 19833748
Arthritis Rheum. 2003 Jan;48(1):54-8
pubmed: 12528103