FRI0051 DURATION OF EXPOSURE TO BIOLOGICS AND STATINS MODERATES THE EFFECTS OF CUMULATIVE INFLAMMATION ON CORONARY ATHEROSCLEROSIS PROGRESSION IN RHEUMATOID ARTHRITIS

Background: Higher inflammatory load associates with increased risk of cardiovascular events in patients with rheumatoid arthritis (RA). We recently reported that occult atherosclerosis burden on coronary computed tomography angiography (CCTA) predicted long-term cardiovascular events (CVE) in RA above and beyond cardiac risk factors or scores. We further showed that higher cumulative inflammatory burden independently predicted coronary plaque progression. Objectives: To explore whether the duration of exposure to biologic DMARDs and/or statins during the study period mitigates the effect of cumulative inflammatory load on coronary plaque progression. Methods: One hundred-one participants with a baseline CCTA underwent a follow-up evaluation in 83±3.6 months. Plaque burden was reported as segment involvement score (SIS, describing the number of coronary artery segments with plaque per patient) and coronary artery calcium (CAC), quantified by the Agatston method. Robust logistic and linear regression models evaluated effects of predictors on plaque (SIS) progression and CAC change, respectively. Predictors of interest were time-averaged c-reactive protein (CRP), duration of bDMARD exposure (years), duration of statin exposure (years), and their 2- and 3-way interactions. Models were controlled for age and baseline hypertension. Significant interactions were subsequently decomposed and examined based on a median split for the duration of biologic and statin exposure. Results: A significant interaction between inflammation and statin exposure duration was observed for plaque progression p=0.019 (figure 1A); in patients with shorter statin exposure ( 1 year) attenuated that effect [OR=1.37, 95% CI=0.67 to 2.82, p=0.391). Notably, significant three-way interactions were observed between time-averaged CRP, duration of bDMARD exposure and duration of statin exposure on plaque progression [p=0.050] and CAC change [p=0.006]. In patients with shorter biologic exposure ( 1 year), inflammation was not related to plaque progression [OR=1.25, 95% CI=0.48 to 3.31, p=0.65] or CAC change [β=-0.16, 95% CI=-0.43 to 0.21, p=0.52]. In patients with longer biologic exposure ( Conclusion: The relationship between cumulative inflammation, length of treatment with bDMARDs, statins and their ultimate impact on coronary plaque progression in RA are highly nuanced. The effect of the duration of statin exposure on coronary plaque burden progression seems relevant only in the context of insufficient biologic exposure; shorter treatment with statins in that setting allows for significant coronary plaque progression in response to higher cumulative inflammatory load. In contrast, longer statin exposure attenuates that risk. Disclosure of Interests: 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