Российский кардиологический журнал (Apr 2021)
Biomarkers of inflammation, parameters characterizing obesity and cardiac remodeling in patients with atrial fibrillation and metabolic syndrome
Abstract
Aim. To determine the blood level of inflammatory markers, parameters characterizing obesity and cardiac remodeling in patients with atrial fibrillation (AF) in combination with metabolic syndrome (MS).Material and methods. This single-stage case-control study included 677 subjects aged 35 to 65 years: patients with MS (n=407), of which 128 patients with AF; comparison group — patients with AF without MS (n=75); control group — practically healthy subjects without cardiovascular diseases and metabolic disorders (n=195).Results. It was found that the blood concentration of circulating pro-inflammatory biomarkers in patients with AF and MS is higher than in patients with AF without MS: C-reactive protein (CRP) (4,43 (2,68-4,98) and 2,33 (1,08-4,7) mg/L, p<0,0001), interleukin-6 (IL-6) (2,5 (1,28-5,13) and 1,27 (0,68-2,7) pg/ml, p<0,0001) and tumor necrosis factor-α (TNF-α) (5,18 (2,63-7,32) and 3,42 (2,115,48) pg/ml, p<0,0001). The serum CRP concentration positively correlates with left (ρ=0,451, p<0,0001) and right atrial (ρ=0,412, p<0,000) volumes, as well as with the waist circumference (ρ=0,503, p<0,001) and epicardial fat thickness (ρ=0,550, p<0,001). Plasma IL-6 and serum TNF-α levels correlated to a lesser extent with parameters characterizing atrial remodeling, but had a strong positive relationship with epicardial fat thickness. According to multivariate analysis, it was found that an increase in the epicardial fat thickness had a greater effect on an increase in blood concentration of CRP, IL-6 and TNF-α, in contrast to other parameters characterizing obesity, such as body mass index and waist circumference.Conclusion. An increase in the blood concentration of proinflammatory biomarkers CRP, IL-6, and TNF-α is associated with cardiac remodeling and epicardial fat thickness in patients with MS and probably has a pathogenetic role in increasing the AF risk in this cohort of patients.
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