Abstract

Objective: to investigate the relationship between some signs of hereditary connective tissue disorders (HCTDs) as a Marfanoid appearance (MA) and the risk of atrial fibrillation (AF) in female patients with osteoporosis (OP). Subjects and methods. In 2014–2015, the investigation enrolled consecutively 104 women aged 58 to 70 years (mean age, 64.7±3.8 years) who had a verified diagnosis of primary OP and a body mass index of ≤25.0 kg/m2. The entries in the outpatient medical records and in the automated information system «Polyclinic» were retrospectively analyzed to divide the patients into 2 groups according to the sign of the documented diagnosis of AF. A study group consisted of 53 women (mean age, 65.6±5.2 years) with AF and OP; a control group included 38 patients (mean age, 64.9±4.7 years) with OP without AF; a control group comprised 38 patients (mean age, 65.1±3.9 years) without OP and AF. Anthropometric and phenotypical parameters and cardiovascular visceral signs were analyzed; the levels of transforming growth factor-β1 (TGFβ1) and interleukin (IL) 1β and 6 in the serum and those of deoxypyridinoline (DPD) in the urine were measured. Results. Analysis of the phenotypical signs of HCTDs in the patients with OP has shown that those with OP and AF have external signs of dysmorphogenesis and meet the criteria of MA. Statistically significant correlations were found between the frequency of MA signs and the magnitude of all cardiac morphometric parameters and the visceral signs of HCTDs in the study group. The serum levels of IL-1β, IL-6, and TGFβ1 in these patients were significantly higher than in the comparison and control groups. There was also a high correlation between the signs of MA and the content of DPD in the study group. Conclusion. The patients with OP and AF was found to have a statistically significant correlation of the phenotypical signs of dysmorphogenesis with the frequency of visceral signs of HCTD, the morphofunctional parameters of the heart, and the high concentration of cytokines and DPD. It may be suggested that there exists a genetically determined mechanism of connective tissue dysembryogenesis in OP, which is associated with the risk of AF.

Highlights

  • Цель исследования – изучение связи между отдельными признаками наследственных нарушений соединительной ткани (ННСТ) в виде марфаноидной внешности (МВ) и риском развития фибрилляции предсердий (ФП) у пациенток с остеопорозом (ОП)

  • The entries in the outpatient medical records and in the automated information system «Polyclinic» were retrospectively analyzed to divide the patients into 2 groups according to the sign of the documented diagnosis of atrial fibrillation (AF)

  • A study group consisted of 53 women with AF and OP; a control group included 38 patients with OP without AF; a control group comprised 38 patients without OP and AF

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Summary

ОРИГИНАЛЬНЫЕ ИССЛЕДОВАНИЯ

Марфаноидная внешность как фактор риска фибрилляции предсердий у пациентов с остеопорозом Золотовская И.А., Давыдкин И.Л. Цель исследования – изучение связи между отдельными признаками наследственных нарушений соединительной ткани (ННСТ) в виде марфаноидной внешности (МВ) и риском развития фибрилляции предсердий (ФП) у пациенток с остеопорозом (ОП). The patients with OP and AF was found to have a statistically significant correlation of the phenotypical signs of dysmorphogenesis with the frequency of visceral signs of HCTD, the morphofunctional parameters of the heart, and the high concentration of cytokines and DPD. Уточнение взаимосвязи ННСТ с заболеваниями костно-мышечной и сердечно-сосудистой системы для прогнозирования развития ФП у пациентов с ОП представляется весьма актуальным. Цель исследования – оценка связи между отдельными признаками ННСТ в виде МВ и риском развития ФП у пациентов с ОП. Проведен ретроспективный анализ записей в медицинской карте амбулаторного больного, а также в автоматизированной информационной системе «Поликлиника» с целью разделения пациенток на две группы по признаку документально подтвержденного диагноза ФП (шифр I48 по МКБ-10).

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