Полиморфные варианты G/C+915 трансформирующего фактора роста бета 1 и фибрилляция предсердий у пациентов с метаболическим синдромом

Objective . Metabolic syndrome (MS) increases the risk of atrial fibrillation (AF). The probability of the incident AF increases in case of atrial fibrosis and remodeling. Transforming growth factor beta 1 (TGF-β1, encoding gene TGFB1) induces myocardial fibrosis, in particular, in the atria. We analyzed the distribution of CC, CG and GG genotypes G/C+915 polymorphism of TGFB1 gene in patients with MS and AF. Design and methods . We included 426 subjects (30–65 years old): 222 patients with MS, including 115 patients with paroxysmal and permanent AF. The control group included 209 healthy individuals without cardiovascular disease and metabolic disorders. Genomic DNA was isolated from the venous blood. Allelic variants were identified by polymerase chain reaction followed by restriction analysis with endonucleases BglI. Results . GG genotype G/C (+915) TGFB1 gene in patients with MS and AF is more frequent than in MS patients without AF (97,4 and 87,9 %, respectively; χ 2 = 6,19, p = 0,013) and in healthy individuals (97,4 and 86,6 %, respectively; χ 2 = 8,77, p = 0,003). GG genotype is associated with an increased the risk of AF in patients with MS (odds ratio (OR): 5,74, 95 % confidence interval (CI): 1,71–19,33, p = 0,012). There were no differences in GG genotype G/C (+915) TGFB1 gene in MS patients without AF and healthy individuals. GC genotype G/C (+915) TGFB1 gene in healthy individuals was found more frequently than in MS with AF (12,4 and 2,6 %, respectively; χ 2 = 7,63, p = 0,006) and more frequently in MS patients without AF (12,1 and 2,6 %, respectively; χ 2 = 6,19, p = 0,013). C allele (genotype GC+CC) gene TGFB1 is associated with the decreased risk of AF in patients with MS (OR = 0,19, 95 % CI 0,05–0,70, р = 0,001). Conclusions . We found an association of G/C (+915) TGFB1 gene with the risk of AF in patients with MS. C allele (СС and CG genotypes) seems to be protective and is associated with the 5,3-fold reduction in the risk of AF in patients with MS. We suggest that increased expression of gene TGFB1 causes heterogeneity of conduction and contributes to the AF in patients with MS.