Endogenous estrogen exposure and cardiovascular mortality risk in postmenopausal women (original) (raw)
Related papers
Life Sciences, 2019
Duration of endogenous estrogen exposure is apparently associated with risk of cardiovascular disease, the longer durations being more cardiovascular disease protective in women. We aimed to investigate the association of cumulative duration of endogenous estrogen exposure over women's reproductive lifespans with cardiovascular disease outcomes. Main methods For the purpose of the present study, of 10192 female participants, after excluding those using HRT (n=84), 3656 women, aged ≥ 30 years, who met eligibility criteria were selected and divided into three groups based on tertiles (T1,T2,T3) of exposure durations to endogenous estrogen. Cox proportional hazards regression model was used to estimate associations between exposure durations and cardiovascular disease outcomes. Key findings Cardiovascular events occurred in 352 participants over a median follow-up of 14.2(13.5, 14.6) years (7.7 per 1000 person years; 95%
Severity of cardiovascular disease in women: Relation with exposure to endogenous estrogen
Maturitas, 2006
Objectives: Coronary artery disease (CAD) is more common in men than in women. Endogenous sex steroids may be the main factor responsible, as long-term estrogen action appears to be protective. The aim of the study was to investigate the predisposing factors responsible for the severity of CAD in women. Methods: One hundred and eight women (100 menopausal) undergoing coronary angiography were studied. Reproductive function was recorded. The severity of CAD was assessed by the number of arteries with severe stenosis, the presence of angina and myocardial infarctions (MI). Results: The time since menopause (TSM) was significantly longer in women with angina and with MIs compared to those without (20.3 ± 8.7 years versus 15.8 ± 8.7 years and 22.6 ± 8.6 years versus 18.1 ± 8.9 years, p < 0.05), independently of chronological age. The age at menopause was significantly younger in women who had 2 MIs compared to those with 1 or 0 MI (41.5 ± 3.5, 47.5 ± 5.3 and 48.4 ± 5.4 years, respectively; p = 0.04); the total duration of menstrual cyclicity was inversely related to the number of MIs (35.6 ± 5.8, 34.2 ± 5.3 and 28.3 ± 3.3 years, 0, 1 and 2 MIs, respectively; p = 0.03). Conclusions: The severity of CAD in women referred for coronary angiography is correlated with measures of exposure to endogenous estrogen. Both the TSM and the age at menopause are aggravating factors for MI, independently of age. There is an independent protective effect of the duration of estrogen exposure on the number of MIs; this has not been reported before and supports the protective role of the length of exposure to endogenous estrogen, especially for the occurrence of MI in this selected group of women.
International Journal of Cardiology, 2008
Background: The aim of the present study was to investigate the added value of age at menopause and the lifetime cumulative number of menstrual cycles in cardiovascular risk prediction in postmenopausal women. Methods: This study included 971 women. The ankle-arm index was used as a proxy for cardiovascular morbidity and mortality. The ankle-arm index was calculated for each leg by dividing the highest ankle systolic blood pressure by the highest brachial systolic blood pressure. A cut-off value of 0.95 was used to differentiate between low and high risk women. Three cardiovascular risk models were constructed. In the initial model all classical predictors for cardiovascular disease were investigated. This model was then extended by age at menopause or the lifetime cumulative number of menstrual cycles to test their added value for cardiovascular risk prediction. Differences in discriminative power between the models were investigated by comparing the area under the receiver operating characteristic (ROC) curves. Results: The mean age was 66.0 (± 5.6) years. The 6 independent predictors for cardiovascular disease were age, systolic blood pressure, total to HDL cholesterol ratio, current smoking, glucose level, and body mass index ≥ 30 kg/m 2 . The ROC area was 0.69 (0.64-0.73) and did not change when age at menopause or the lifetime cumulative number of menstrual cycles was added. Conclusions: The findings in this study among postmenopausal women did not support the view that age at menopause or a refined estimation of lifetime endogenous estrogen exposure would improve cardiovascular risk prediction as approximated by the ankle-arm index.
International Journal of Cardiology, 2008
Heart disease is a major cause of illness and death in women. It is well known that there is an increase in cardiovascular disease and cardiovascular risk factors after the menopause, but it is still unclear whether the change in risk factors after the menopause is only related to the aging process or is principally due to estrogen deprivation. Observational studies suggest a protective role for estrogens, whereas recent randomized controlled trials report a negative effect of oral estrogens on primary and secondary prevention of cardiovascular events.
The Lancet Public Health, 2019
Background Early menopause is linked to an increased risk of cardiovascular disease mortality; however, the association between early menopause and incidence and timing of cardiovascular disease is unclear. We aimed to assess the associations between age at natural menopause and incidence and timing of cardiovascular disease. Methods We harmonised and pooled individual-level data from 15 observational studies done across five countries and regions (Australia, Scandinavia, the USA, Japan, and the UK) between 1946 and 2013. Women who had reported their menopause status, age at natural menopause (if postmenopausal), and cardiovascular disease status (including coronary heart disease and stroke) were included. We excluded women who had hysterectomy or oophorectomy and women who did not report their age at menopause. The primary endpoint of this study was the occurrence of first non-fatal cardiovascular disease, defined as a composite outcome of incident coronary heart disease (including heart attack and angina) or stroke (including ischaemic stroke or haemorrhagic stroke). We used Cox proportional hazards models to estimate multivariate hazard ratios (HRs) and 95% CIs for the associations between age at menopause and incident cardiovascular disease event. We also adjusted the model to account for smoking status, menopausal hormone therapy status, body-mass index, and education levels. Age at natural menopause was categorised as premenopausal or perimenopausal, younger than 40 years (premature menopause), 40-44 years (early menopause), 45-49 years (relatively early), 50-51 years (reference category), 52-54 years (relatively late), and 55 years or older (late menopause). Findings Overall, 301 438 women were included in our analysis. Of these 301 438 women, 12 962 (4•3%) had a first nonfatal cardiovascular disease event after menopause, of whom 9369 (3•1%) had coronary heart disease and 4338 (1•4%) had strokes. Compared with women who had menopause at age 50-51 years, the risk of cardiovascular disease was higher in women who had premature menopause (age <40 years; HR 1•55, 95% CI 1•38-1•73; p<0•0001), early menopause (age 40-44 years; 1•30, 1•22-1•39; p<0•0001), and relatively early menopause (age 45-49 years; 1•12, 1•07-1•18; p<0•0001), with a significantly reduced risk of cardiovascular disease following menopause after age 51 years (p<0•0001 for trend). The associations persisted in never smokers, and were strongest before age 60 years for women with premature menopause (HR 1•88, 1•62-2•20; p<0•0001) and early menopause (1•40, 1•27-1•54; p<0•0001), but were attenuated at age 60-69 years, with no significant association observed at age 70 years and older. Interpretation Compared with women who had menopause at age 50-51 years, women with premature and early menopause had a substantially increased risk of a non-fatal cardiovascular disease event before the age of 60 years, but not after age 70 years. Women with earlier menopause need close monitoring in clinical practice, and age at menopause might also be considered as an important factor in risk stratification of cardiovascular disease for women.
Cardiovascular Risk During the Menopause
Vascular Disease Prevention, 2009
Although initial experimental data and results of observational studies suggest that hormone replacement therapy (HRT) is associated with a reduction in the risk of heart disease, the results for events such as stroke or thromboembolism are less clear. Randomized secondary and primary prevention studies have found that HRT is not protective against the risk of coronary heart disease, stroke or progression of atherosclerosis. Therefore, HRT therapy should not be initiated to prevent vascular disease among postmenopausal women. There are numerous explanations for the divergent findings of observational and randomized clinical trials of HRT. For example, study design and differing biological effects of HRT on vascular risk factors. The use of HRT for young postmenopausal women with moderate to severe menopausal vasomotor symptoms appears to be safe. The absolute risk of vascular event associated with HRT is low and varies depending on factors like age or years since the menopause. The presence or absence of cardiovascular risk factors determines the differences in vascular risk linked to HRT. Further studies should identify the mechanisms involved and determine whether and how different regimens of HRT influence vascular risk as well as the influence of individual patient characteristics.