OP0090 THE OCCURRENCE OF SUBCLINICAL AND CLINICAL ATHEROSCLEROSIS IN RHEUMATOID ARTHRITIS, RESULTS FROM THE 3-YEAR, MULTICENTER, PROSPECTIVE, OBSERVATIONAL, GIRRCS STUDY

Background The systemic inflammatory process and the “traditional” cardiovascular (CV) risk factors could synergize the enhancement of CV burden in rheumatoid arthritis (RA) [1]. Objectives To assess the occurrence and the predictive factors of subclinical and clinical atherosclerosis in patients with RA. Methods During 2015, consecutive patients, admitted to Italian Rheumatology Units, were assessed in GIRRCS (Gruppo Italiano di Ricerca in Reumatologia Clinica e Sperimentale) cohort [2]. After that, patients were followed-up in a 3-year, prospective, observational study, assessing the occurrence of subclinical (carotid and/or peripheral arteries atherosclerotic lesions detected by ultrasound imaging) and clinical atherosclerosis (myocardial infarction and/or congestive heart failure and/or cerebrovascular accidents) 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. Results After 3 years of prospective follow-up, 797 patients (82.7% female, median age of 60 years, range 21-89) were assessed. We also observed a median RA duration of 8.35 years (range 0.1-35), 70.9% of patients showed rheumatoid factor and 55.7% ACPA. Among “traditional” CV risk factors, we observed that BMI was 27.21 ± 4.05, 33% of patients reported smoking habit, 49.3% were affected by high blood pressure (HBP) and 12.3% by type 2 diabetes (T2D). Corticosteroids were administered in 75.5% of patients (low dosage 66.8%), methotrexate in 86.8%, hydroxychloroquine in 28.1% and biologic DMARDs in 60.7%. The remission was reached and maintained in 42.6% of patients, during the follow-up. We recorded an increased rate of subclinical atherosclerosis (70 vs 130 patients p Conclusion The maintenance of remission was strongly associated with a reduced risk of clinical and subclinical atherosclerosis in 3-year prospective follow-up. Among “traditional” CV risk factors, T2D was significantly associated with both clinical and subclinical atherosclerosis. References [1] Nurmohamed MT, et al. Nat Rev Rheumatol. 201511:693-704 [2] Ruscitti P, et al. Medicine (Baltimore). 2017;96:e8180. Disclosure of Interests Piero Ruscitti Grant/research support from: PFIZER INNOVARE 2018, Speakers bureau: MSD, BMS, SOBI, LILLY, PFIZER, Paola Cipriani Grant/research support from: ACTELION, Speakers bureau: ACTELION, Vasiliki Liakouli Grant/research support from: PFIZER, Speakers bureau: SANOFI, Daniela Iacono Speakers bureau: PFIZER, Ilenia Pantano: None declared, Giulia Maria Destro Castaniti: None declared, Nicola Maruotti Speakers bureau: N Maruotti has received speaker honoraria from Pfizer outside this work, Domenico Paolo Emanuele Margiotta: None declared, Licia Picciariello: None declared, Francesco Caso: None declared, Rosa Daniela Grembiale Grant/research support from: BMS, Consultant for: JANSSEN, CELGENE, Speakers bureau: PFIZER, JANSSEN, BMS, NOVARTIS, Fabiola Atzeni: None declared, Raffaele Scarpa Speakers bureau: ABBVIE, MSD, PFIZER, LILLY, JANSEEN, CELGENE, Federico Perosa Speakers bureau: OCCASIONALLY, Antonella Afeltra Grant/research support from: MSD, PFIZER, ABBVIE, ROCHE, UCB, Speakers bureau: MSD, PFIZER, BMS, ROCHE, SANOFI, Francesco Paolo Cantatore Speakers bureau: PFIZER, ROCHE, Giuliana Guggino Grant/research support from: Laborest, Pfizer, Consultant for: Novartis, Abbvie, Speakers bureau: Sandoz, Francesco Ciccia Grant/research support from: CELGENE, PFIZER, Consultant for: UCB, NOVARTIS, CELGENE, PFIZER, LILLY, Paid instructor for: UCB, NOVARTIS, CELGENE, PFIZER, LILLY, JANSSEN, Speakers bureau: UCB, NOVARTIS, CELGENE, PFIZER, LILLY, JANSSEN, ROCHE, AMGEN, Roberto Giacomelli Grant/research support from: Pfizer, Actelion, Speakers bureau: Actelion, Bristol-Myers Squibb, Merck Sharp & Dohme, Abbvie, Pfizer, Sobi, Roche