SAT0544 CORONARY PLAQUE PROGRESSION IN RHEUMATOID ARTHRITIS: ROLE OF INFLAMMATION, CARDIAC RISK FACTORS, MEDICATIONS AND IMPACT ON EVENT RISK
Authors: George Karpouzas, Sarah Ormseth, Elizabeth Hernandez, Matthew Budoff
Journal: Annals of the Rheumatic Diseases (2019)

<h3>Background</h3> Patients with Rheumatoid Arthritis (RA) exhibit higher prevalence, burden and different composition of occult coronary plaque compared with age and gender-matched controls. Moreover, plaque burden on coronary computed tomography angiography (CCTA) predicted long-term cardiovascular events (CVE) in RA beyond cardiac risk factors or scores. <h3>Objectives</h3> To evaluate change in coronary plaque burden and composition, predictors thereof and its impact on CVE risk in RA. <h3>Methods</h3> One hundred-one participants with a baseline CCTA underwent a follow-up evaluation in 83±3.6 months. Plaque load was reported as segment involvement score (SIS-number of segments with plaque); segment stenosis score (SSS- cumulative stenosis over all evaluable segments) and total plaque score (TPS- collective plaque amount over all segments). Plaque composition was defined as non-calcified (NCP), mixed (MP) or calcified (CP). Coronary artery calcium (CAC) was quantified by the Agatston method. Robust logistic regression models evaluated predictors of increased plaque burden compared to non-progression. Independent predictors entered as continuous variables included age, time-averaged c-reactive protein (CRP), cumulative prednisone dose, bDMARD exposure (years), and statin exposure (years). Gender, hypertension, dyslipidemia, diabetes, and presence of IgA anti-beta2-glycoprotein1 antibodies (a-b2GPI-IgA) constituted dichotomous independent variables. Cox proportional hazards models assessed the role of SIS, SSS, TPS and CAC progression on incident CVE risk 14±2.7 months later, after adjustment for cardiac risk scores, or baseline plaque load. <h3>Results</h3> Total plaque burden increased in 42% of patients; progression was predicted by older age, higher cumulative inflammation (TA-CRP) and higher total prednisone dose (table 1). Longer exposure to bDMARDs and statins was linked to lower risk of NCP progression (all p&lt;0.05). MP change was predicted by a-b2GPI-IgA presence, whereas CP progressors were older, more obese, hypertensive and with higher cumulative inflammation compared to non-progressors (p&lt;0.05). CAC increase correlated with older age, hypertension, obesity, higher inflammation and a-b2GPI-IgA presence (Table 1). Both total plaque and CAC progression predicted CVE independently of baseline burden and cardiac risk scores (all p≤0.014). <h3>Conclusion</h3> Change in coronary atherosclerosis burden and consistency was differentially impacted by Inflammation, cardiac risk factors, a-b2PI-IgA presence and medications such as prednisone, biologics and statins and independently predicted cardiovascular events in RA. <sup>¶</sup>p&lt;0.1, *p&lt;0.05, **p&lt;0.01, ***p&lt;0.001 <h3>Disclosure of Interests</h3> George Karpouzas Grant/research support from: Pfizer, Consultant for: Sanofi-Genzyme-Regeneron, Janssen, Roche-Genentech, Pfizer, Speakers bureau: BMS, Sanofi-Genzyme-Regeneron, Janssen, Roche-Genentech, Sarah Ormseth: None declared, Elizabeth Hernandez: None declared, Matthew Budoff: None declared