IgA antibodies to phosphocholine associate with long-term cardiovascular disease risk
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CitationKankaanpää, J. Sämpi, M. Bloigu, R. Wang, C. Akhi, R. Kesäniemi, YA. Remes, AM. Ukkola, O. Hörkkö, S. (2018). IgA antibodies to phosphocholine associate with long-term cardiovascular disease risk. ATHEROSCLEROSIS, 269, 294-300. 10.1016/j.atherosclerosis.2017.12.010.
Background and aims
Antibodies to phosphocholine and oxidized LDL (oxLDL) are proposed to modify progression of atherosclerosis. We investigated the prognostic value of antibodies to phosphocholine (PCho), Streptococcus pneumoniae cell wall polysaccharide (CWPS) and oxLDL in defining long-term CVD survival.
CVD incidence was followed for 18 years and analyzed with baseline plasma IgM, IgG and IgA antibody levels to PCho, CWPS and oxLDL in 1044 subjects of Oulu Project Elucidating Risk of Atherosclerosis study (OPERA).
During the follow-up period, 195 subjects (18.7%) had a CVD event. Cox model with ACC/AHA CVD adjustments (ASCVD) showed that IgA levels to PCho and IgA to CWPS were statistically significant factors predicting CVD risk. IgM and IgG antibodies to PCho, CWPS and oxLDL had no effect on CVD risk after adjusting for other risk factors. Net reclassification improvement (categories: 17-year risk <15%, 15–30%, >30%), was 0.06 (−0.001–0.12, p < 0.054), and IDI was 0.0124 (0.0036–0.0211, p < 0.006) with IgA-PCho added to the ASCVD risk model. Seventeen (9.4%) study subjects with CVD events were correctly reclassified into higher risk category while 9 (5.0%) subjects were classified into lower risk category. Among the non-cases, 58 (8.7%) subjects were correctly reclassified into lower risk, and 46 (5.9%) were reclassified into higher risk category.
Plasma IgA antibodies to PCho and Streptococcus pneumoniae CWPS are significant predictors of long-term CVD risk. Additional studies on the role of IgA antibodies in atherogenesis and CVD are warranted.
Subjectsphosphocholine Streptococcus pneumoniae antibody cardiovascular disease biomarker
Link to the original itemhttp://dx.doi.org/10.1016/j.atherosclerosis.2017.12.010
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