МЕТАБОЛІЧНІ ПОРУШЕННЯ У ЖІНОК, ХВОРИХ НА НЕСТАБІЛЬНУ СТЕНОКАРДІЮ, ЗАЛЕЖНО ВІД ЗВИЧКИ КУРІННЯЛьвівський національний медичний університет імені Данила ГалицькогоРезюме. Куріння -один з основних факторів ри-зику розвитку гострих форм ішемічної хвороби серця. Обстежено 65 хворих на нестабільну стенокардію жі-нок-курців і некурців. Встановлено, що в жінок-курців спостерігається достовірно гірший метаболічний ста-тус, а саме: підвищення загального холестерину, холес-терину ліпопротеїдів низької густини, холестерину ліпопротеїдів дуже низької густини, тригліцеридів, активності перекисного окиснення ліпідів, зниження вмісту холестерину ліпопротеїдів високої густини. Се-ред жінок-курців більша частка хворих на цукровий діабет. Водночас виявлено пошкоджувальний вплив куріння на мікроциркуляторне русло у вигляді змен-шення швидкості клубочкової фільтрації. Спостеріга-лась тенденція до підвищення рівня сечової кислоти і γ-глютамілтранспептидази.Ключові слова: нестабільна стенокардія, жінки-курці, жінки-некурці, ліпідний, вуглеводний, пурино-вий обмін.Вступ. Серцево-судинні захворювання (ССЗ) -найбільш часта причина смерті серед жінок у світі, яка складає третину всіх смертель-них випадків [9]. За даними одного з останніх оглядів National Health and Nutrition Examination Surveys (NHANES), за останні два десятиліття розповсюдженість ССЗ у жінок віком 35-54 роки збільшилась, у той час як у чоловіків того ж віку вона знизилась [13]. Аналізуючи показники смертності в Україні, автори відзначають її ріст у 2013р. від гострих і підгострих форм ішемічної хвороби серця (ІХС) [2].Виявлено більше 100 факторів ризику розви-тку ІХС. До найбільш агресивних факторів, які прискорюють розвиток ІХС, належать артеріаль-на гіпертензія, гіперхолестеринемія та тютюнопа-ління. При їх комбінації ризик коронарної смерті зростає у 8 разів. Куріння -один із провідних стимулів структурних і функціональних змін сер-ця і судин. У світі нараховується 1,5 млрд курців, причому біля 5,5 млн вмирають від захворювань, пов'язаних із тютюнопалінням [3].Особливо небезпечним щодо кардіоваскуля-рного здоров'я є куріння у жінок [5,6]. Дослі-дження, проведене в Японії, під час якого протя-гом десяти років проводилося спостереження за станом здоров'я 88613 жінок, які не хворіли на цукровий діабет (ЦД), показало, що на тлі курін-ня серцево-судинний ризик зростав у середньому на 39 %, при цьому додатковий ризик внаслідок куріння в середньому віці був навіть вищим, ніж у літньому [8].Негативний вплив куріння саме на жіночий організм є серйознішим завдяки здатності сигаре-тного диму зменшувати продукування та пору-шувати метаболізм екстрагенів, що мають кардіо-протективну дію [5]. Поширеність куріння серед жінок за останні 30 років потроїлась, наслідком чого є зростання метаболічних порушень, часто-ти розвитку гострих форм ІХС, зокрема нестабі-льної стенокардії (НС) [1,13]. Незважаючи на чисельні наукові роботи, які присвячені вивчен-ню процесів ліпідного, вуглеводного і пуриново-го обміну при ССЗ, залишаються невирішеними питання безпосередньої ролі куріння в цих мета-б...

The aim of the study. To study the effect of smoking on lipid metabolism, lipid transport system and systemic inflammation, to find out their correlations and the risks of unstable angina in women, depending on the habit of smoking.Material and methods. 225 women were examined: 150 women - patients with unstable angina and 75 healthy women. The level of total cholesterol, low and high-density lipoprotein cholesterol, triglycerides, apolipoproteins A1 (ApoA1) and B (ApoB), C-reactive protein, fibrinogen were determined in all subjects. Multifactor correlation-regression analysis was performed using Fisher's test. Statistical processing of the results was performed using the applications "Microsoft Office Excel 2016" and "Statistics ver. 10.Results. The relative risk of developing unstable angina in patients with a smoking habit is most often associated with atherogenic dyslipidemia (total cholesterol > 4 mmol, OR = 12.02, SI = 8.12-16.32; low-density lipoprotein cholesterol > 1.8 mmol / l, OR = 9,32, SI = 6,13-12,56, high-density lipoprotein cholesterol <1,2 mmol / l, OR = 3,91, SI = 2,12-5,45, the ratio of apolipoproteins ApoV / ApoA1> 0.85, OR = 2.69, SI = 1.15-4.21) and the highest activity of systemic inflammation (C-reactive protein >3 mg / l, OR = 3.62, SI = 2.15- 4.56). The risk of developing unstable angina associated with these indicators is 1.5-2 times higher in women with a smoking habit than in women who have never smoked. Significant direct correlations of high and medium strength between the severity of systemic inflammation, disorders of the lipid transport system (increase in the ratio of ApoB / ApoA1 and decrease in the level of ApoA1), in patients with unstable angina in women smokers.Conclusions. Smoking is one of the most aggressive factors of unstable angina in women, which contributes to the emergence and progression of other important risk factors and leads to disorders of lipid metabolism, lipid transport system, systemic inflammation and increased chances of unstable angina.

The aim of the study: to determine the prevalence, interrelation and prognostic value of the major risk factors (RF) of unstable angina (UA) in women, depending on smoking habits.Materials and methods. 225 women (average age 53.80 ± 6.47 years) were examined: 150 women were patients with UA (group I) and 75 healthy women (group II). Depending on the smoking factor, all women were subdivided into subgroups: A (smokers, IA -patients with UA (n = 86), IIA -almost healthy (n = 45)) and B (non-smokers, IB -patients with UA (n = 64)), IIB were almost healthy (n = 30). The examination included an identification of major RF (hypertension, diabetes mellitus, obesity, dyslipidemia (DLP), measurement of total cholesterol, low-density lipoprotein cholesterol (LDL) and high density (HDL), apolipoprotein A1 (ApoA1) and apolipoprotein B (ApoB), C-reactive protein (CRP), fibrinogen (FG), transforming growth factor (TGF-β2), endothelin-1 (ET-1), endothelial NO synthase (eNOS), malonic dialdehyde (MDA), ceruloplasmin (CP). In order to assess the impact of RF on the development of UA, a multifactorial correlation and regression analysis was performed using the Fisher test.Results. Female smokers (IA) were significantly 1.4-2.5 times more likely to have such RF as hypertension, diabetes mellitus, DLP and obesity than non-smokers (IB), as well as a combination of ≥3 RF (84.9 % vs. 62.5 %) and ≥5 RF (34.9 % vs. 13.9 %). Smoker patients showed severe disorders of lipid metabolism, higher activity of systemic inflammation and endothelial dysfunction. In female smokers (IA), the relative risk of developing UA was associated (P < 0.05) with DLP ((total cholesterol ˃4 mmol (OR = 12.02, CI = 8.12-16.32), LDL ˃1.8 mmol/l (OR = 9.32, CI = 6.13-12.56), HDL ˂1.2 mmol/l (OR = 3.91, CI = 2.12-5.45)), hypertension (OR = 3.49, CI = 2.96-4.25); endothelial dysfunction (ET-1 ˃7.87 pg/ml (OR = 7.44, CI = 2.89-6.21); eNOS ˂180 pg/ml (OR = 3.42, SI = 2.16-4.78); TGF-β2 <168 pg/ml (OR = 4.13; CI = 2.78-5.92)), systemic inflammation and peroxidation activity (CRP ˃3 mg/l (OR = 3.62, CI = 2.15-4.56), MDA ˃0.45 nmol/mg (OR = 2.89, CI = 1.55-3.91), CP ˃380 mg/year (OR = 2.34, CI = 1.46-3.25). Risks of UA development with regard to the above indicators was 1.5-2 times higher in female smokers (IA) compared to nonsmokers (IB), which might account for UA occurrence approximately 8 years earlier in female smokers (IA) than in non-smokers (IB). A strong multiple correlation was found between TGF-β2 and ET-1 (R = 0.60, at Р = 0.000003), as well as a high predicted risk of UA associated with ˃12 smoking years, ET-1 levels ˃30 pg/ml, TGF β2 ˂145 pg/ml, body mass index ˃30 units and CRP ˃14 mg/l.

Introduction. Smoking is one of the most aggressive risk factors for acute coronary heart disease (CHD), especially in women. The number of women smokers in Ukraine has tripled in the last 30 years. Women smokers, even with heavy smoking, are 7 times more likely to suffer from corticosteroids. The issues of the peculiarities of lipid metabolism disorders, lipid transport system and systemic inflammation in practically healthy women, depending on the smoking habit, have not been studied enough, and therefore are the aim of our study. The aim of the study. To find out the features of disorders of lipid metabolism, lipid transport system and systemic inflammation in almost healthy women, depending on the habit of smoking. Materials and methods. 75 women were involved to the study. Depending smoking habit, all subjects were divided into two groups: almost healthy women smokers (n = 45, mean age 52.78 ± 2.52 years) – experimental group (EG), almost healthy women non-smokers (n = 30, mean age 54.81 ± 3.21 years) – comparison group. To determine the peculiarities of the state of lipid metabolism, the state of the lipid transport system, the activity of systemic inflammation, all subjects were determined indicators of total cholesterol, low-density lipoprotein cholesterol (LDL cholesterol), high-density lipoprotein cholesterol (HDL cholesterol), apolipoproteins A1 (ApoA1), apolipoproteins B (ApoB), calculated the ratio of ApoB / ApoA1, C-reactive protein (CRP) and fibrinogen (FB). Results. It was found that the content in the serum of cholesterol in almost half (48.89 %) of women with a habit of smoking, was greater than 4.50 mmol/l. The mean rate of total cholesterol among these individuals was 5.84 ± 0.05 mmol/l, which was significantly higher than in the cohort of comparison group women with total cholesterol more than 4.50 mmol/l who did not have a smoking habit. Similar trends were observed in the case of comparing the proportions of individuals with LDL cholesterol more than 3.00 mmol/l. In particular, this excess was registered in 31.11 % in women with smoking habit, which is significantly (1.33 times) higher than in women with the comparison group (23.33 %). In contrast, the proportion of surveyed women with a reduced less than 0.96 g/l ApoA1 in women with smoking habit was significantly 1.62 times higher than in the women from the comparison group (37.78 % vs. 23.33 %, p less than 0.05). Also, among these individuals, the average ApoA1 was lower in smokers than among non-smokers (0.91 ± 0.04 g/l vs. 0.96 ± 0.03 g/l, p less than 0.05). The calculation of the ApoB/ApoA1 ratio showed a higher intensity of proatherogenic shift of the lipid spectrum in smokers. Female smokers percentage of persons with a CRP greater than 3.00 mg/ml was 13.34 %, which is twice as much (p less than 0.05) than in the group of non-smokers, in which there were 6 such persons, 6.67 %. Conclusions. Disorders of lipid metabolism, lipid transport system and systemic inflammation in women depending on the habit of smoking have their own characteristics – in women smokers, these disorders are significantly more severe than in women without smoking, and are atherogenic, namely: significantly higher levels of total cholesterol, cholesterol low-density lipoproteins, triglycerides, apolipoprotein B transport proteins, apolipoprotein B / apolipoprotein A1 transport protein ratios, mean values of C-reactive protein and fibrinogen, and lower levels of high-protein lipoprotein A1 protein and high protein lipoproteins.

The aim — to improve the diagnosis and treatment of unstable angina (UA) in female smokers based on the study of clinical features, lipid and carbohydrate metabolism, markers of inflammation and endothelial dysfunction and their relationship.Materials and methods. 225 women were examined, including 150 patients with UA (group I) and 75 women of comparable age without signs of coronary heart disease (group II). The groups identified subgroups A (smokers) and B (non‑smokers). The main risk factors were identified: arterial hypertension (AH), diabetes mellitus, obesity, dyslipidemia (DLP), total cholesterol (TC), low density lipoprotein (LDL) cholesterol and high density lipoprotein (HDL) cholesterol, triglycerides, apolipoproteins A1 (ApoA1) and apolipoproteins B (ApoB), C‑reactive protein (C‑RP), fibrinogen, transforming growth factor (TGF‑b2), endothelin‑1 (ET‑1), endothelial NO synthase (eNOS), malondialdehyde, ceruloplasmin. To assess the influence of risk factors on the development of UA, a multivariate correlation and regression analysis was performed using the Fisher criterion. To study the effectiveness of quercetin in the standard treatment complex of UA in women with/without a smoker status, an analysis of the dynamics of its clinical course, lipid and carbohydrate metabolism, and systemic inflammation, markers of endothelial dysfunction and lipid peroxidation was conducted on the 1st and 10th day of treatment.Results and discussion. In smoking women with UA compared with women of a similar age without coronary heart disease, incidence of hypertension, diabetes mellitus, DLP and obesity, combination of ≥ 3 risk factors (84.9 and 62.5 %) and ≥ 5 risk factors (34.9 and 13.9 %), statistically significantly higher levels of total cholesterol, LDL cholesterol, triglycerides, ApoB, the ratio of ApoB/ApoA1 and low levels of HDL cholesterol and ApoA1 was recorded 1.4 — 2.5 times more often. The severity of these disorders was directly proportional to the intensity of smoking. In female smokers, the presence of UA was associated (p < 0.05) with DLP (OXS > 4 mmol (relative risk (RR) — 12.02, 95 % confidence interval (CI) — 8.12 — 16.32), LDL cholesterol > 1.8 mmol/l (RR 9.32; 95 % CI 6.13 — 12.56), HDL cholesterol < 1.2 mmol/l (RR 3.91; 95 % CI 2.12 — 5.45)), hypertension (RR 3.49; 95 % CI 2.96 — 4.25), endothelial dysfunction (ET‑1 > 7.87 pg/ml (RR 7.44; 95 % CI 2.89 — 6.21), eNOS < 180 pg/ml (RR 3.42; 95 % CI 2.16 — 4.78), TGF‑b2 < 168 pg/ml (RR 4.13; 95 % CI 2.78 — 5.92)), activity of systemic inflammation and peroxidation (C‑RP > 3 mg/l (RR 3.62; 95 % CI 2.15 — 4.56), malondialdehyde > 0.45 nmol/mg (RR 2.89; 95 % CI 1.55 — 3.91), ceruloplasmin > 380 mg/(l · h) (RR 2.34; 95 % CI 1.46 — 3.25)). Smoking women with UA, unlike women who do not smoke, showed a strong multiple correlation between TGF‑b2, ET‑1 and smoking (R = 0.60, p = 0.000003). A high predicted risk of developing UA with tobacco smoking > 12 years, ET‑1 > 30 pg/ml, TGF‑b2 < 145 pg/ml, body mass index > 30 kg/m2 and C‑RP > 14 mg/l was established. In women smokers who were additionally prescribed quercetin, a statistically significantly (1.4 — 1.7 times) positive dynamics of the above indicators was recorded both in comparison with smokers who received only the recommended therapy and non‑smokers who were prescribed quercetin.Conclusions. The development of unstable angina in female smokers occurs under conditions of a high activity of systemic inflammation and free radical oxidation and a low level of endothelial protection. Quercetin as part of standard therapy improves the treatment of unstable angina in female smokers.