Unstable angina in female smokers: features of clinical course and treatment optimization

Abstract

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.