POS0214\u2005ASSOCIATION BETWEEN C-REACTIVE PROTEIN AND 10-YEAR RISK OF CARDIOVASCULAR DISEASE IN RHEUMATOID ARTHRITIS USING THE ERS-RA SCORE: A CROSS-SECTIONAL ANALYSIS OF THE CORDIS COHORT

Abstract

Rheumatoid arthritis (RA) is associated with an increased risk of atherosclerotic cardiovascular disease (CVD). The Expanded Cardiovascular Risk Prediction Score for Rheumatoid Arthritis (ERS-RA) estimates the 10-year risk of myocardial infarction, stroke or CVD-related death based on conventional and RA-specific (clinical disease activity index, CDAI, disease duration, glucocorticoid use) risk factors (1).We evaluated the associations between ERS-RA 10-year risk of CVD, high-sensitivity C-reactive protein (hs-CRP) concentrations, and pharmacological treatment in 1,251 RA patients collected by the “Cardiovascular Obesity and Rheumatic Disease Study (CORDIS)” group of the Italian Society of Rheumatology (SIR).We assessed independent associations between ERS-RA risk score and each relevant variable using multivariate regression (ENTER approach; listwise deletion analysis). Given the relatively high number of missing hs-CRP data (n=385), regression analysis was also performed using multiple imputation (10 sets, Stata 16.1). Regression models were not adjusted for independent variables included in the ERS-RA score.Among 1,251 RA patients [mean (SD) age 60.4(9.3), range (40-80) years; 78% female; mean (SD) disease duration, 11.6(8) years; mean (SD) CDAI, 9(9); mean (SD) HAQ, 0.77(0.7); mean (SD) hs-CRP, 6.8(12) mg/L] the estimated 10-year CVD risk was 11.6(0.9) % [mean (SD)]. Regarding treatment, 539(43%) received glucocorticoids, 676(54%) a biological or targeted synthetic disease-modifying anti-rheumatic drug (b/tsDMARD) (n missing=1), and 885(81%) at least one conventional synthetic DMARD (csDMARD). Ninety-three (7.4%) patients did not receive any treatment. After adjusting for the use of b/tsDMARD and csDMARD, hs-CRP concentrations were significantly associated with 10-year risk of CVD both in standard multiple regression (n=865; coefficient=0.005 for each 10\u2009mg/L hs-CRP increment, 95% confidence interval (0.000-0.100), p=0.043) and after multiple imputation (n=1,251; coefficient=0.005 for each 10\u2009mg/L hs-CRP increment, 95% confidence interval (0.000-0.114), p=0.035) (Table 1). This corresponds to an increase of 10-year CV risk of 1% for every 20\u2009mg/L increase in hs-CRP concentrations.In a large cohort of RA patients, we observed a significant, positive, and independent association between hs-CRP concentrations and 10-year CV risk estimated by ERS-RA. The cross-sectional design of the study did not allow to establish a cause-effect relationship between hs-CRP and CV risk. Given that conventional CV risk factors and inflammation-related variables are accounted for in the ERS-RA risk score, other, unexplored, mechanisms may underlie the observed association between hs-CRP and CV risk.[1]Solomon, D. H., et al. “Derivation and internal validation of an expanded cardiovascular risk prediction score for rheumatoid arthritis: a Consortium of Rheumatology Researchers of North America Registry Study.” Arthritis & rheumatology 67.8 (2015): 1995-2003.Table 1.Multiple regression modelsModel 1n= 865Model 2n= 1, 251ERS-RA scoreCoefficient95% CI, pCoefficient95% CI, phs-CRP, every 10\u2009mg/L increment0.0050.000 to 0.100, 0.0430.0050.000 to 0.011, 0.035b/tsDMARD use-0.002-0.005 to 0.001, 0.199-0.000-0.002 to 0.002, 0.963csDMARD use0.002-0.003 to 0.007, 0.3940.002-0.002 to 0.006, 0.371Prob >F, model with only CRP0.030.03Prob >F, full model0.070.08A multiple linear regression (ENTER method) was performed for the dependent variable ERS-RA score using a listwise deletion analysis (Model 1) and a multiple imputation analysis (Model 2).None declared