B-po04-137 soluble st-2 levels are elevated in patients with atrial fibrillation

Studies show the association between inflammatory chemokines and atrial fibrillation (AF). Factors, such as CRP, IL-6 and TNF-α, are a few that are well-known to be increased in AF patients. However, there is a paucity of knowledge regarding sST2, a soluble isoform of ST2, known to prevent the NF-κB cell signaling pathway, in AF. To study the relationship between specific chemokines and AF, confirming known inflammatory chemokine associations (CRP, IL-6, MMP2, VCAM-1) and investigating novel ones (sST2). Between July 2018 and June 2019, blood was drawn from consenting subjects 18 to 89 years of age with AF, other atrial arrhythmias, or other cardiovascular disease from a single institution. Patients with congenital heart disease, and end-stage renal disease on hemodialysis, were excluded. Plasma samples were sorted into patients with and without AF. The following chemokines were measured by flow cytometry using the BioLegend LEGENDplex Flow Assay Kit and compared between subjects with and without AF: MCP-1, IL-1B, TNF-α, sST2, IF-γ, VEGF, adiponectin, CRP, MMP2, leptin, I-CAM1, VCAM-1, MMP9. A two-sample t-test was used to compare the groups. Soluble ST2 was significantly higher in AF patients (n=51, 1033 ng/mL, p-value <0.0001) than those without AF (n=65, 862.8 ng/mL). Uniquely, I-CAM1 (AF 868.3 ng/mL, No AF 1146 ng/mL, p-value 0.02), leptin (AF 9227 ng/mL, No AF 14607 ng/mL, p-value 0.01), and IF-γ (AF 20.76, No AF 28.67 ng/mL, p-value <0.0001) were reduced in patients with AF. As expected, IL-6 (AF 17.06 ng/mL, No AF 9.74 ng/mL, p-value <0.0001), CRP (AF 16477 ng/mL, No AF 6547 ng/mL, p-value <0.0001), VCAM-1 (AF 155299 ng/mL, no AF 104246 ng/mL, p-value 0.001), and MMP-2 (AF 224195 ng/mL, No AF 147037 ng/mL, p-value 0.0003) were significantly higher in AF patients. Certain signaling chemokines may predict high risk of developing AF and/or target AF interventions in the future. Interestingly, sST2 is significantly higher in AF patients, though other inflammatory counterparts, such as I-CAM1, leptin and IF-γ, have an inverse association. This suggests that while certain inflammatory ligands may precipitate AF, others may have a protective role.