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- Ajeganova, S, et al.
(författare)
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Carotid atherosclerosis, disease measures, oxidized low-density lipoproteins, and atheroprotective natural antibodies for cardiovascular disease in early rheumatoid arthritis -- an inception cohort study
- 2012
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Ingår i: The Journal of rheumatology. - : The Journal of Rheumatology. - 0315-162X .- 1499-2752. ; 39:6, s. 1146-1154
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Tidskriftsartikel (refereegranskat)abstract
- Although an enhanced risk of cardiovascular disease (CVD) in persons with rheumatoid arthritis (RA) is well established, the mechanisms behind it remain unclear. We studied whether carotid atherosclerosis, RA disease measures, or potential cardiovascular biomarkers influenced the incidence of CVD in an RA inception cohort.Methods.RA disease measures and CVD biomarkers were assessed at 0, 3, 12, 24, and 60 months after disease onset, and carotid ultrasonography after 5 years. The study outcome was incident CVD events — acute myocardial infarction, angina pectoris, congestive heart failure, or ischemic cerebrovascular event. Survival analysis and Cox and longitudinal regressions were used for statistical analyses.Results.A total of 105 patients, without CVD events prior to RA onset, experienced 17 CVD events, an incidence rate of 1.35 events per 100 person-years (95% CI 0.71–2.0). The rate of CVD events did not differ with regard to measures of carotid intima-media thickness, but it was higher for patients with bilateral carotid plaques than for those without (p = 0.012). Improvement in Disease Activity Score for 28 joints, visual analog scale for pain, and Stanford Health Assessment Questionnaire score over the first year, as well as usage of methotrexate (MTX), was associated, independent of age, with reduction of risk of CVD event [hazard ratios 0.68 (95% CI 0.5–0.97), 0.97 (95% CI 0.95–0.99), 0.35 (95% CI 0.15–0.82), and 0.34 (95% CI 0.12–0.91), respectively]. In longitudinal analyses, increasing oxidized low-density lipoprotein (oxLDL) and probability for low antiphosphorylcholine antibodies (anti-PC) were observed in those who experienced a subsequent CVD event.Conclusion.Bilateral carotid plaques were associated with poor CVD-free survival. Early reductions of inflammation, pain, and disability as well as MTX usage were associated with better CVD outcome. Elevated oxLDL and low IgM anti-PC levels may link chronic inflammation in RA to enhanced risk of CVD events.
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- Ajeganova, S, et al.
(författare)
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HIGHER LEVELS OF NATURAL ANTI-PHOSPHORYLCHOLINE ANTIBODIES ARE ASSOCIATED WITH LOWER RISK OF INCIDENT CARDIOVASCULAR EVENTS IN YOUNGER PATIENTS WITH RHEUMATOID ARTHRITIS
- 2020
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Ingår i: ANNALS OF THE RHEUMATIC DISEASES. - : BMJ. - 0003-4967 .- 1468-2060. ; 79, s. 939-939
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- The increased cardiovascular (CV) risk in rheumatoid arthritis (RA), especially in seropositive RA, is not fully explained by traditional risk factors. Immuno-inflammatory mechanisms and autoantibodies could be involved in the pathogenesis of atherosclerotic disease. Recent studies have suggested that anti-phosporylcholine antibodies (anti-PC) of IgM subclass counteract the generation of senescent and IL-17+ T-cells, have atheroprotective effects and may play a role in formation and stabilization of atherosclerotic plaque.Objectives:To investigate the association between IgM anti-PC antibodies with cardiovascular (CV) morbidity in patients with RA in age and sex groups and by serostatus.Methods:The study population was derived from the BARFOT early RA cohort, recruited in 1994-1999. The outcome was CV events i.e. AMI, angina pectoris, coronary intervention, ischemic stroke and TIA tracked through the Swedish Hospital Discharge and the National Cause of Death Registries. The RA-disease measures and traditional risk factors were assessed according to the protocol. Sera collected at inclusion and the 2-year visit were analyzed with ELISA to determine levels of anti-PC IgM (Athera CVDefine kit, Athera Biotechnologies AB). The Kaplan-Meier estimates and Cox proportional-hazards regression models were applied. Analysis were stratified by median level of IgM anti-PC and performed within strata of age, sex and RA-autoantibodies.Results:In all, 654 patients with early RA, 68% women, mean (SD) age 55(14.7) years, DAS28 5.2(1.3), 60% RF-positive and 60% ACPA-positive without prevalent CVD were included in this analysis. The level of IgM anti-PC at baseline was median (IQR) of 60.9(36.4-94.9) and at 2 years 56.0(32.3-84.2) U/ml. During follow-up of > 10 years, 141 incident CV events (21.6%) were registered. The levels of anti-PC both at inclusion and after 2 years of observation were lower in participants who experienced CV event than in those who did not, p=0.020 and p=0.012.The CV event-free survival differed between patients with levels of anti-PC above median compared with those with levels below, p=0.003 by log-rank test. The risk for incident CV event showed a 0.6-fold hazard (95% CI, 0.4-0.8) among patients with higher anti-PC levels as compared with those with lower levels, p=0.003. In the age groups, the risk for incident CV event was lower in patients aged <55 years at inclusion than in those who were older, hazard ratio (HR) 0.40 (0.17-0.94), p=0.036. This result persisted when adjusted for sex and all traditional risk factors, HR 0.36 (0.14-0.92), p=0.032. Also, the risk for incident CV events was lower in patients with higher anti-PC levels in females, HR 0.61 (0-39-0.45), and double RF- and ACPA- negative patients, 0.44 (0.21-0.90), in crude analyses.The favourable effect of anti-PC at baseline and the CV outcome was not observed in ages >55 years, males, ACPA+ and RF+ patients. There were no significant association between anti-PC level at 2 years and outcome.Conclusion:These results suggest that higher levels of IgM anti-PC are associated with a lower risk of incident CV events over 10 years in younger patients. The favourable atheroprotective effect of IgM anti-PC may be a part of explanation of lower risk of atherosclerotic disease in younger persons, females and in those with seronegative RA.Acknowledgments :6th Framework Program of the European Union (grant LSHM-CT-2006-037227 CVDIMMUNE)Disclosure of Interests:Sofia Ajeganova: None declared, Maria Andersson: None declared, Johan Frostegård Grant/research support from: Unconditional competitive grant from Amgen, related only to PCSK9, not the topic of this abstract, Ingiäld Hafström: None declared
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