Aim:To assess the value of body mass index (BMI) and adipokine levels in predicting development of atrial fibrillation (AF) in the general population. Methods: Three hundred and ninety eight patients were examined for the presence of phenotype metabolically healthy obesity (MHO), according to the Wildman criteria; adipokine levels were assessed by enzyme immunoassay method; AF was assessed by electrocardiography (ECG) and/or by ECG diurnal monitoring. Results: Obesity (group 1) and overweight (group 2) was present in 23.7% and 42.0% of participants; while 21.1% were normal body weight (group 3) and 13.1% had a BMI < 19.9 kg/m² (group 4). Phenotype MHO was detected in 19.6% patients. At follow-up, 32.4% of participants developed AF. Adiponectin levels were significantly higher in MHO patients as compared to metabolically unhealthy patients with abdominal obesity (AO). High molecular weight adiponectin (HMVAN) levels were significantly decreased in patients of groups 1 and 4, as compared to groups 2 and 3. Correlation between AF and HMWAN was determined by regressive analysis in patients of 1st and 4th groups (β = -0.24, P = 0.003 and β = -0.26, P = 0.002, respectively). Conclusion: The probability of developing AF increases with AO and decreased BMI, which is accompanied by a change in HMVAN levels. In MHO patients, the probability of AF developing is identical with persons having normal BMI.
Key words:Atrial fibrillation, obesity, metabolically healthy obesity, metabolically unhealthy obesity, serum leptin, high-molecular-weight adiponectin
ABSTRACTArticle history:
Purpose: to investigate the effect of hormonal changes on endothelial dysfunction (ED) in patients with a comorbid course of hypertension (H), type 2 diabetes mellitus (T2DM) and subclinical hypothyroidism (SHT). Methods: 183 patients with H stage II were divided into 3 groups: Group 1 (n=50) -with isolated H (comparison group); Group 2 (n=63) -with a combined course of H and T2DM; Group 3 (n=70) -with comorbidity of H, T2DM and SHT. Blood pressure levels, carbohydrate, lipid and thyroid metabolism, plasma insulin concentration, insulin resistance (IR) the HOMA-IR index, vascular endothelial growth factor (VEGF-A) plasma levels were investigated. Results: Dyslipidemia was more pronounced in group 2 than in group 1. The addition of SHT was accompanied by a tendency to increase all the atherogenic lipids. IR was observed in all patients groups and was significantly higher than in control group (p<0.05). Significant increase of VEGF-A levels in all patients groups in comparison with the control (p<0.05) was found. In group 2 VEGF-A was lower than in group 1, which is probably due to the protective effect of metformin. Analysis of the influence of thyroid dysfunction degree on ED revealed significant increase of VEGF-A levels in TSH>6.0 ?MU/ml subgroup (352.55±17.64 pg/ml vs 461.74±20.13 pg/ml (p<0.05)). Conclusion: Hormonal disorders contribute to aggravation of endothelial dysfunction in patients with hypertension and comorbid endocrinopathies -type 2 diabetes mellitus and subclinical hypothyroidism. Even minor decrease in thyroid function lead to the progression of endothelial dysfunction.
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