Risks of developing unstable angina in female smokers

Abstract

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.

Conclusions. Smoking is one of the most aggressive factors of unstable angina in women, contributing to the appearance and progression of other major risk factors, which leads to systemic inflammation, peroxidation, endothelial dysfunction and increases the chances of acute coronary heart disease occurrence even in relatively young women.