Abstract 15089: Specificity for Inflammatory Pathways and Myocardial Injury Associated With Coronary Microvascular Dysfunction in Rheumatoid Arthritis

Background: Coronary microvascular disease (CMD) is associated with increased mortality in rheumatoid arthritis (RA). Studies suggest that higher RA disease activity is associated with a higher degree of CMD. However, it is not known whether specific inflammatory pathways implicated in RA play a stronger role than others in the pathogenesis of CMD. The objective of this study was to identify the associations between inflammatory cytokines, CMD, and resultant myocardial injury. Methods: We used baseline data from the first 53 subjects enrolled in a study of RA and CV risk (LiiRA, NCT02714881). LiiRA enrolls RA patients, age>35, prior to TNF inhibitor initiation. All subjects underwent a stress myocardial perfusion PET scan to quantify coronary flow reserve (CFR). CFR is the ratio of myocardial blood flow during maximal hyperemia over that at rest. A lower CFR in the absence of obstructive coronary artery disease (CAD) is indicative of CMD. We tested the association between markers of inflammation and myocardial injury with CFR using the Spearman correlation. Results: Clinical characteristics of LiiRA subjects are shown in Table 1. Baseline cardiac risk factors were uncommon. IL-6, sTNFR2, NT-proBNP were correlated with lower CFR. However, no significant associations were observed between IL-1β, hsCRP, or hs-cTnT (Table 2). Conclusions: Among RA patients with no history of overt CAD, the severity of CMD was correlated with IL-6 and sTNFR2 but not IL-1β or hsCRP. CMD was further associated with increased levels of NT-proBNP but not hs-cTnT. These findings provide potential insight into the mechanisms by which inflammation mediates CMD and resultant myocardial dysfunction.