Severity of cardiovascular disease in women: Relation with exposure to endogenous estrogen (original) (raw)
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EMAS position statement: Managing the menopause in the context of coronary heart disease
Maturitas, 2011
Introduction: Cardiovascular disease (CVD) including coronary heart disease (CHD) and stroke is the most common cause of female death. Premenopausal CHD is very rare but when women enter the menopause the incidence of CHD increases markedly. CHD presents 10 years later in women than in men. The reason is still unclear but the protective effects of estrogens have been suggested. Aims: To formulate a position statement on the management of menopause women in the context of coronary heart disease. Materials and methods: Literature review and consensus of expert opinion. Results and conclusions: Based on long term randomized placebo-controlled studies hormone therapy (HT) is not recommended for the primary or secondary prevention of CHD in postmenopausal women. In most countries the only indication for HT is the treatment of menopausal symptoms. Women with known CHD or with many coronary risk factors seeking HT because of troublesome climacteric symptoms should be evaluated for their individual baseline risk of developing breast cancer, venous thromboembolism and CHD recurrence. The same applies to non hormone therapy-based treatments where long term clinical studies are lacking. Risks should be weighed against expected benefit from symptom relief and improved quality of life. The lowest effective estrogen dose should be used during the shortest possible time. Transdermal administration is preferred if risk factors for VTE exist. Different progestogens might differ in their cardiovascular effects. Observational studies suggest that micronized progesterone or dydrogesterone may have a better risk profile than other progestogens with regard to thrombotic risk.
Endogenous estrogen exposure and cardiovascular mortality risk in postmenopausal women
American journal of …, 2002
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. Am J Epidemiol 2002;155:339-45.
Journal of Women's Health, 2009
Objective: It has been suggested that both endogenous reproductive hormones and hormone therapy may play a protective role against coronary artery disease (CAD). However, recent clinical trials have failed to demonstrate the benefit of a variety of forms of hormone therapy. The observational data on the role of endogenous reproductive hormones, using surrogate measures such as number of birth, age at menarche, and age at menopause are inconsistent. In addition, the longer-term associations have not been evaluated. The aim of this study was to evaluate the relationships between detailed measurements of endogenous and exogenous estrogen exposure time with angiographic CAD and major adverse cardiovascular events. Methods: We assessed total estrogen exposure time, quantitative CAD by a core angiography laboratory, and prospectively measured major adverse cardiovascular events in 646 postmenopausal women undergoing coronary angiography for evaluation for suspected ischemia in the Women's Ischemia Syndrome Evaluation (WISE) study. Results: Timing of postmenopausal exogenous hormone therapy (HT) use was associated with reduced CAD. Two summarized total estrogen time scores (TET and sTET) were not related to angiographic CAD after accounting for HT use. In addition, these scores were not related to cardiovascular events over a median of 6.0 years of follow-up. Conclusions: There was no independent relation of estrogen exposure time to angiographic CAD or major adverse cardiovascular events in a contemporary cohort of postmenopausal women evaluated for suspected ischemia. Our results suggest that the paradigm of estrogen protection from CAD in women may be more complex than estrogen exposure duration alone.
Gesundheitswesen, 2015
Ischemic heart disease (IHD) is the number one health threat to women in the USA. While significant advances in femalespecific symptoms and pathophysiology have begun to improve mortality rates, a closer look at risk factors across a woman's lifespan needs to be explored. This review targets three time frames: premenopause, pregnancy and postmenopause. During premenopause, menstrual cycle patterns and estrogen status provide information for IHD risk. Pregnancy conditions provide another window of time that potentially contributes to future cardiovascular risk. Lastly, there is a rise in IHD events and mortality after menopause. Research continues to decipher the impact of estrogen decline at this stage and the effect of menopause hormone therapy as they relate to the cardiovascular health of menopausal women.
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.
Maturitas, 2006
Randomised clinical trials find no protection against development of ischaemic heart disease by use of Hormone Therapy (HT) after the age of 50 years. Observational studies suggest that early menopause is a risk factor for ischaemic heart disease. Yet, a clinical very relevant question is whether HT reduces this risk associated with early menopause. Objective: To analyse whether early menopause based on various causes are independent risk factors for ischaemic heart disease, and to investigate whether the risks are modified by use of HT. Methods: In a prospective cohort study questionnaires were mailed to Danish female nurses above 44 years of age in 1993. Information on menopause, use of HT and lifestyle was obtained. In total 19,898 (86%) nurses fulfilled the questionnaire, among them 10.533 were postmenopausal with definable menopausal age, free of previous ischaemic heart disease, stroke or cancer. Through individual linkage to national register incident cases of ischaemic heart disease were identified until end of 1998. Results: Menopause below both age 40 and 45 was associated with an increased risk of ischaemic heart disease, seeming most pronounced for women who had an early ovariectomy but also among spontaneous menopausal women. Generally HT did not reduce the risk except for the early-ovariectomised women, where no increased risk of ischaemic heart disease for HT users was found.
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%
Maturitas, 2010
Premenopausal women have a relatively lower risk of ischemic heart disease (IHD) compared to age matched men and this gender gap narrows after menopause. The observation that the onset of IHD occurs 10 years later in women than it does in men is said to suggest that endogenous reproductive hormones play a protective role. Indeed, animal models and human epidemiological studies suggest that oophorectomy is a risk factor for accelerated IHD. In animal models, hormone therapy (HT) has anti-atherosclerotic effects after oophorectomy, HT in the form of oral contraceptives (OCs) prevents atherosclerosis in anovulatory cycling women, and large numbers of premenopausal women taking OCs have relative safety from an IHD standpoint (1). Further, observational epidemiological studies in humans have consistently demonstrated protective effects for IHD among HT users. Such studies are typically performed on relatively younger women where HT is prescribed for vasomotor symptoms during menopausal transition or shortly following menopause. In contrast, clinical trials in older, postmenopausal and often asymptomatic women have demonstrated no overall benefit and early adverse effects when randomized to a variety of forms of HT (1). These data discrepancies have called into question the validity of the reproductive hormone estrogen protection hypothesis, and raise the alternative possibility