Plasma IgM inversely correlates with coronary artery AS risk 2335222

Abstract Introduction B cells are important immune cells in murine atherosclerosis (AS), regulating lesion development in a subset-dependent manner. B-2b cells promote atherosclerosis while B-1b cells and marginal zone B cells (MZB) exert atheroprotective effects largely through the production of IgM antibodies. IgM is thought to limit AS through clearance of harmful oxidative byproducts in plaques and recognition of immunogenic oxidation specific epitopes. IgM has been shown to inversely associate with coronary artery AS severity. Yet, whether IgM levels are associated with early indices of AS like coronary artery calcium (CAC) and coronary computed tomography angiography (CCTA) risk score (CRS) is unknown. We investigated the relationship between total IgM levels and imaging risk scores in a human cohort. Based on previous work, we hypothesize an inverse relationship. Methods We performed enzyme-linked immunosorbent assay (ELISA) for total IgM levels on plasma samples from 318 subjects in the Coronary Assessment in Virginia (CAVA) cohort, who underwent CCTA to obtain CAC and CRS measurements. CRS which considers which severity and spatial extent of coronary plaque and CAC score, which measures calcium deposits in arteries, are predictors of cardiovascular risk. Multivariate and Univariate analysis were measured in R and further correlated in PRISM. Results Univariate analysis demonstrated that plasma IgM levels did not correlate with traditional AS risk factors such as hypertension, diabetes, hyperlipidemia, BMI, and smoking history. Plasma IgM levels did correlate inversely with the CRS (r=-0.931, p = 0.022) and CAC score (r=-0.0070, p = 0.049). The inverse relationship between CRS and IgM was retained for multivariate analysis (r=-0.878, p = 0.043). Conclusion Our data indicates that higher plasma IgM is associated with lower cardiovascular risk in early AS, suggesting it may have potential as a biomarker in human populations that could benefit from early risk factor modification. Funding Source Leducq Foundation, NIH R01 AI172112 Topic Categories Basic Autoimmunity (BA)