Abstract

Objective: To determine the concentration of blood fibrotic and inflammatory biomarkers in patients with atrial fibrillation (AF) associated with metabolic syndrome (MS) components. Design and method: The study included 646 patients aged 35–65 years: patients with AF and MS (n = 142), those with AF and without MS (n = 113), those with MS and without AF (n = 175) and the control group consisted of healthy subjects without cardiovascular and metabolic diseases (n = 107). All participants underwent anthropometric and laboratory investigations. Profibrogenic (aldosterone, galectin-3, TGF-beta1, CTGF) and proinflammatory (CT-1, IL-6) factors were determined in serum and plasma by ELISA. Results: The highest concentrations of fibrotic and inflammatory biomarkers were found in patients with AF in combination with MS. In MS patients without AF, the concentration of aldosterone, galectin-3, TGF-beta1, CTGF, CT-1, and IL-6 was also higher than in healthy subjects. In patients with AF and hypertension (HTN), but without abdominal obesity (AO), higher values of aldosterone (108,1 ± 70,3 pg/ml and 89,3 ± 32,2 pg/ml, p = 0,003) and TGF¬beta1 (3680,1 ± 1863,3 pg/ml and 1968,1 ± 1611,5 pg/ml, p = 0,015) in serum than in AF patients without HTN and without AO. In the group of patients with AF and AO, but without HTN, higher concentrations of IL-6 (2,9 ± 0,7 pg/ml and 1,9 ± 0,6 pg/ml, p = 0,001) and CTGF (162,9 ± 92,2 pg/ml and 116,3 ± 63,4 pg/ml, p = 0,0001). Correlation analysis made it possible to establish a stronger relationship between aldosterone and TGF¬beta1 with systolic blood pressure (r = 0,493, p < 0,0001 and r = 0,530, p < 0,0001), and CT¬1, CTGF and IL¬6 in a greater degree correlated with waist circumference (r = 0,563, p < 0,0001; r = 0,626, p < 0,0001; r = 0,480, p < 0,0001). Conclusions: It can be assumed that hypertension through the aldosterone system and TGF-beta1, as well as abdominal obesity through the cytokine system CT-1 and IL-6 activate various mechanisms and pathways for myocardial emodelling. Integral molecules galectin-3 and CTGF mediate their interactions, in particular in patients with a combination of several MS components and contribute to a higher AF risk.

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