Menopausal transition enhances the atherogenic risk of smoking in middle aged women.

BACKGROUND: The presence of cardiovascular risk factors during the menopausal transition could be critical in the development of atherosclerosis. In the present study, we evaluated whether the menopausal transition has impact on traditional and newly discussed risk factors. METHODS: Six hundred ninety nine women from population-based study underwent ultrasound measurement of the intima-media thickness of the common carotid arteries (CIMT) - Prague Pre and Postmenopausal Females study (3PMFs). In addition, 40 women selected according to reproductive and smoking status were examined with regard to number of circulating endothelial progenitor cells, markers of reverse cholesterol transport and sex hormones, including their fluctuation - Hormone Variability study (HVs). RESULTS: Age, smoking, body mass index, systolic blood pressure and HDL cholesterol were independently associated with the CIMT in 3PMFs group. The increase in the CIMT with age was markedly steeper in current/past smokers than in non-smokers among perimenopausal women (p for equality of slopes=0.005). This difference was not observed in premenopausal and menopausal women. In the HVs group, endothelial progenitor cells and reverse cholesterol transport were substantially higher while triglycerides and fluctuation of free testosterone were lower in non-smokers than in smokers in menopausal transition. In contrast, in menopausal women, the fluctuation of free testosterone was higher in non-smokers; no other differences between smokers and non-smokers were detected. CONCLUSIONS: These results suggest that atherogenic effect of smoking may be enhanced during menopausal transition. The mechanism could be impaired reparative vascular processes, impaired reverse cholesterol transport and rapidly changing status of sex hormones.

Blood pressure around the menopause: a population study.

BACKGROUND: Hypertension is a major cardiovascular risk factor possibly explaining the excessive cardiovascular morbidity and mortality in postmenopausal women. Cross-sectional and longitudinal studies have explored this issue with diverging results. Our study sought to elucidate the impact of the menopause on blood pressure in a representative population sample. METHODS: The study involved randomly selected 908 female residents of a Prague district, aged 45-54 years (respondence rate, 63.9%). Three definitions of the menopause were used: self-reported menstrual characteristics (premenopausal with the final menstrual period less than 60 days; late menopausal transition, with final menstrual period 60-365 days; and postmenopausal, final menstrual period more than 365 days before the examination), levels of follicle-stimulating hormone (< or = 40 IU/l for premenopausal and more than 40 IU/l for postmenopausal women), and both. RESULTS: Age-adjusted and BMI-adjusted systolic blood pressure and diastolic blood pressure did not differ among the groups regardless of the definition of menopause. There was also no difference in the prevalence of hypertension and in the age-adjusted and BMI-adjusted odds ratio for hypertension. Multiple regression analysis testing the association between systolic blood pressure and diastolic blood pressure, and age, BMI, heart rate, smoking, and antihypertensive medication explained a rather small proportion of the BP variation. No correlation was found between BP and age in either subgroup; the closest correlation was always found between BP and BMI. CONCLUSION: In our rather homogeneous representative population random sample of women around the menopause, the rise in blood pressure after the menopause appeared to be due to increased BMI rather than to ovarian failure per se.