Beta-2-glycoprotein-I IgA antibodies predict coronary plaque progression in rheumatoid arthritis

Objectives: To evaluate whether anti-Beta-2-Glycoprotein-I (anti-beta 2GPI) IgA antibodies associate with progression of coronary atherosclerosis and cardiovascular disease (CVD) events in rheumatoid arthritis (RA). Methods: One hundred-fifty patients underwent plaque evaluation (total, non-calcified, mixed and calcified) with coronary computed tomography angiography; 101 were re-imaged within 6.9 +/- 0.3 years to assess progression. The Framingham-D'Agostino score assessed cardiovascular risk. Coronary artery calcium (CAC) and segment involvement score quantified plaque burden. Results: Anti-beta 2GPI IgA were seen in 45 (30%) patients. Despite no link to baseline plaque burden, anti-beta 2GPI IgA associated with segment involvement score increase (adjusted-RR-1.64 [95%CI 1.02-2.63]), CAC change (adjusted-beta=0.33 [95%CI 0.002-0.656]) and developing new extensive or obstructive plaque at follow-up (adjusted-OR-4.24 [95%CI 1.30-13.87]). Adding anti-beta 2GPI IgA to logistic regression models with conventional risk factors predicting plaque progression outcomes increased Area under the receiver-operator curve and improved Net Reclassification and Integrated Discrimination Improvement indices (all P<0.05). In persegment analyses, anti-beta 2GPI IgA predicted mixed plaque formation (adjusted-OR-3.20 [95%CI 1.01-10.09]) and lower likelihood of transition of mixed to calcified plaque (adjusted-OR-0.19 [95%CI 0.04-0.96]). Anti-beta 2GPI IgA moderated the effect of C-reactive protein on CAC change such that C-reactive protein associated with CAC change (beta=0.26 [95%CI 0.14-0.38]) and CVD risk (adjusted-HR-1.89 [95%CI 1.02-3.51]) only in anti-beta 2GPI IgA positive patients. Conclusion: Anti-beta 2GPI IgA addition to clinical risk models improved prediction accuracy of CAC, plaque progression and transition to extensive obstructive disease. They associated with new high-risk mixed plaques and delayed healing to calcified lesions. Anti-beta 2GPI IgA further modified the effect of inflammation on plaque progression and CVD events. (C) 2020 Elsevier Inc. All rights reserved.