We conclude that a consensus concerning the assessment of IMT is urgently needed. Variability of IMT measurements is lowest when determining the mean thickness in the common carotid artery in different directions.

Background Although an association of occurrence of menopause and subsequent oestrogen deficiency with increased cardiovascular disease has been postulated, studies on this association have not shown convincing results. We investigated whether age at menopause is associated with cardiovascular mortality risk. MethodsWe studied a cohort of 12 115 postmenopausal women living in Utrecht, Netherlands, aged 50-65 years at enrolment in a breast cancer screening project. During follow-up of up to 20 years the women attended screening rounds at which we asked questions on menopausal status, age at menopause, medication use, cardiovascular risk factors, and ovarian function. Deaths were ascertained from the patient's family physicians. Life-table analysis and Cox regression analysis were used to investigate the association between age at menopause and cardiovascular mortality. All analyses were adjusted for biological age.Findings 824 women died of cardiovascular causes. 1459 women had left the study area. The risk of cardiovascular mortality was higher for women with early menopauses than for those with late menopauses. The age-adjusted hazard ratio of age at menopause was 0·982 (95% Cl 0·968-0·996, p=0·01)—ie, for each year's delay in the menopause the cardiovascular mortality risk decreased by 2%. The extra risk of early menopause seemed to decrease with biological age (p for interaction 0·07); at biological age 60 the reduction of the annual hazard was 3%, but at age 80 there was no reduction. Adjustment for known cardiovascular risk factors and indicators of ovarian function did not significantly alter the risk estimate.Interpretation These results support the hypothesis that longer exposure to endogenous oestrogens protects against cardiovascular diseases. The effect of an early menopause may be more important at younger biological ages.

These results demonstrate that NO is a potent inhibitor of platelet adhesion under flow conditions and thereby contributes to the regulatory role of vascular endothelial cells on platelet-vessel wall interaction.

In patients with manifest vascular disease the presence of the metabolic syndrome is associated with advanced vascular damage.

In this study, the authors investigated whether combined information on reproductive factors has additive value to the single reproductive factor age at menopause for assessing endogenous estrogen exposure and cardiovascular mortality risk in postmenopausal women. They conducted a population-based cohort study that included 9,450 postmenopausal women from Nijmegen, the Netherlands, who were aged 35--65 years at enrollment in 1975, with a median follow-up of 20.5 years. A Cox proportional hazards model and Receiver Operating Curves were used to analyze the data. Women aged 52 years or more at menopause had an 18% reduction in cardiovascular mortality (hazard ratio = 0.82, 95% confidence interval (CI): 0.69, 0.98) compared with those aged 44 years or less. Women with more than 18 years of exposure to endogenous estrogen had a statistically significant 20% reduction in cardiovascular mortality (hazard ratio = 0.80, 95 percent CI: 0.67, 0.96) compared with those who had 13 years of exposure or less. The area under the curve of the Receiver Operating Curves for the two models was identical (area under the curve = 0.67, 95 percent CI: 0.66, 0.68). This study shows that age at menopause is related to cardiovascular disease mortality and that a newly developed composite measure of endogenous estrogen exposure does not add to the predictive value of age at menopause for cardiovascular mortality.