Key result
Epicardial adipose tissue thickness (OR 2.21; 95% CI 1.11-4.39) and TGF-beta1 (OR 1.01; 95% CI 1.01-1.02) were significant risk factors for atrial fibrillation in metabolic syndrome.
Why the study?
Are epicardial adipose tissue thickness and TGF-beta1 levels associated with atrial fibrillation and left atrial fibrosis in patients with metabolic syndrome?
Cross-Sectional (n=258)
Are epicardial adipose tissue thickness and TGF-beta1 levels associated with atrial fibrillation and left atrial fibrosis in patients with metabolic syndrome?
Odds Ratio: 2.21 (95% CI 1.111–4.386)
p-value: p=0.024
Increased epicardial adipose tissue thickness and elevated TGF-beta1 levels are associated with left atrial fibrosis and a higher risk of atrial fibrillation in patients with metabolic syndrome.
Hypothesis-generating in cross-sectional data; leaves open whether epicardial fat or TGF-beta1 predict incident AF or warrant intervention in metabolic syndrome.
Objective. To determine the relationship between the thickness of epicardial adipose tissue (EAT) and the serum concentration of transforming growth factor beta1 (TGF-beta1) with the severity of left atrial myocardial fibrosis in patients with metabolic syndrome (MS) and to define the role of these factors in atrial fibrillation (AF) development. Design and methods. The study included 258 patients: patients with MS without AF (n = 57), patients with MS and AF (n = 83), patients with AF without MS (n = 36), and otherwise healthy subjects without cardiovascular disease and metabolic disorders (n = 82). Serum level of TGF-beta1 was assessed by ELISA. Epicardial adipose tissue thickness (EAT) was measured by ultrasound on the Vivid 7 apparatus (General Electric, USA). To assess fibrosis we constructed anatomical and amplitude maps of the left atrium (LA) using the non-fluoroscopic electro-anatomical mapping system CARTO3 (Biosense Webster, USA) Results. EAT in patients with MS and AF is higher than in patients with MS without AF (4,7 ± 1,9 and 4,2 ± 1,6 mm, respectively, p = 0,023), higher than in patients with AF without MS (4,7 ± 1,9 and 4,3 ± 1,7 mm, p = 0,01) and significantly higher than in healthy subjects (4,7 ± 1,9 and 2,3 ± 0,9 mm, respectively, p < 0,001). The EAT positively correlated with the percentage of fibrosis of LA estimated by the mapping method (r = 0,549, p < 0,0001). The serum concentration of TGF-beta1 in patients with AF and MS was 6700,2 [2588,4, 17500,3] pg/ml. It was 4,7 times higher than in healthy subjects (p < 0,0001), 2,6 times higher than in patients with MS without AF and higher than in patients with AF without MS. Positive correlations were found between TGF-beta1 and LA volume (r = 0,203, p = 0,03). Binomial regression analysis showed that the probability of AF presence in patients with MS was higher when traditional predictors of this arrhythmia were present — the volume of the LA (odds ratio (OR) = 1,092, 95% confidence interval (CI) 1,026–1,162, p = 0,005), systolic blood pressure (OR = 1,093, 95% CI 1,021–1,169, p = 0,01), as well as EAT (OR = 2,21, 95% CI 1,111–4,386, p = 0,024) and TGF-beta1 (OR = 1,01, 95% CI 1,006–1,015, p = 0,002). Conclusions.Thickness of epicardial adipose tissue and transforming growth factor beta1 are associated with AF also in MS. Probably, epicardial fat and transforming growth factor beta1 stimulate atrial myocardial fibrosis which is the risk factor of AF.
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Zaslavskaya et al. (2018) conducted a cross-sectional in Metabolic syndrome and atrial fibrillation (n=258). Epicardial adipose tissue thickness and TGF-beta1 vs. Healthy subjects and patients without atrial fibrillation or metabolic syndrome was evaluated on Probability of atrial fibrillation presence in patients with metabolic syndrome (OR 2.21, 95% CI 1.111-4.386, p=0.024). Epicardial adipose tissue thickness (OR 2.21; 95% CI 1.11-4.39) and TGF-beta1 (OR 1.01; 95% CI 1.01-1.02) were significant risk factors for atrial fibrillation in metabolic syndrome.
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