Abstract

BackgroundRheumatoid arthritis (RA) is associated with an increased risk of morbidity and mortality, when compared with general population, largely due to enhanced atherosclerotic disease. In this work, we aimed at assessing both occurrence and predictive factors of subclinical and clinical atherosclerosis in RA.MethodsFrom January 1, 2015, to December 31, 2015, consecutive participants with RA, admitted to Italian Rheumatology Units, were assessed in the GIRRCS (Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale) cohort. After that, those participants were followed up in a 3-year, prospective, observational study, assessing the occurrence of subclinical and clinical atherosclerosis and possible predictive factors. McNemar test was employed to assess the changes in subclinical and clinical atherosclerosis, and regression analyses exploited the ORs for the occurrence of those comorbidities.ResultsWe analysed 841 participants, mostly female (82.2%) and with median age of 60 years (range 21–90). The remission was achieved and maintained by 41.8% of participants during the follow-up. We observed an increased rate of subclinical atherosclerosis at the end of follow-up (139 vs 203 participants, p < 0.0001), particularly in participants with a disease duration less than 5 years at baseline (70 participants vs 133 participants, p < 0.0001). Type 2 diabetes (T2D) (OR 4.50, 95%CI 1.74–11.62, p = 0.002), high blood pressure (OR 2.03, 95%CI 1.04–4.14, p = 0.042), ACPA (OR 2.36, 95%CI 1.19–4.69, p = 0.014) and mean values of CRP during the follow-up (OR 1.07, 95%CI 1.03–1.14, p = 0.040) were significantly associated with higher risk of subclinical atherosclerosis. We observed an increased rate of clinical atherosclerosis at the end of follow-up (48 vs 76 participants, p < 0.0001). T2D (OR 6.21, 95%CI 2.19–17.71, p = 0.001) was associated with a significant risk of clinical atherosclerosis. The achievement and the maintenance of remission reduced the risk of subclinical (OR 0.25, 95%CI 0.11–0.56, p = 0.001) and clinical atherosclerosis (OR 0.20, 95%CI 0.09–0.95, p = 0.041).ConclusionsWe reported an increased prevalence and incidence of both subclinical and clinical atherosclerosis in 3-year prospectively followed participants, mainly in the subset with a duration of disease less than 5 years. The achievement and the maintenance of remission are associated with a reduction of the risk of subclinical and clinical atherosclerosis. Among “traditional” cardiovascular risk factors, participants with T2D showed a higher risk of clinical and subclinical atherosclerosis.

Highlights

  • Rheumatoid arthritis (RA) is associated with an increased risk of morbidity and mortality, when compared with general population, largely due to enhanced atherosclerotic disease

  • The achievement and the maintenance of remission are associated with a reduction of the risk of subclinical and clinical atherosclerosis

  • The analysis showed that Type 2 diabetes (T2D), high blood pressure (HBP), anti-citrullinated peptide antibodies (ACPA), remission and mean values of C-reactive protein (CRP) during the follow-up were independently associated with subclinical atherosclerosis

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Summary

Introduction

Rheumatoid arthritis (RA) is associated with an increased risk of morbidity and mortality, when compared with general population, largely due to enhanced atherosclerotic disease. Multiple lines of research are focused on the development of subclinical and clinical atherosclerosis in RA [13, 14] This typical clinical phenotype could result from the synergy between the elevated prevalence of “traditional” cardiovascular (CV) risk factors and inflammation [15]. Some well-known pathogenic pro-inflammatory RA mediators could play a pivotal role in the development of atherosclerosis, as suggested by both pre-clinical and clinical reports [20, 21] In this context, it must be pointed out that the evidence deriving from randomised clinical trials does not entirely clarify this issue. A comprehensive evaluation of CV burden in the RA could be complex as well as timeconsuming, and the identification of biomarkers, accurately reflecting this issue, is still awaited [15, 16, 19, 20, 23]

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