Postmenopausal hormone therapy and cardiovascular disease: An overview of main findings
Section snippets
HT and CHD
The view that HT was considered an effective method to protect postmenopausal women from CHD has been supported by a substantial number of basic science and observational studies. However, recent trials which tested the effect of HT on CHD, failed to confirm this hypothesis.
Observational studies: quantitative overview
Oral estrogen increases VTE risk. This relationship was initially established on the basis of studies of oral contraceptives and was not supported by studies of postmenopausal estrogen replacement. The findings of recent studies of HT differ from studies published earlier that showed no association with VTE. Current data show that HT is associated with a two-to three-fold increased risk of VTE [4]. This risk is higher within the first year of treatment. There is no convincing evidence for a
Conclusion
HT offers well-established clinical benefit for menopausal symptoms but it should not be initiated or continued for the purpose of preventing cardiovascular disease. Certainly, a healthy lifestyle and a good medical care are the basis for preventing cardiovascular disease in postmenopausal women.
Existing trials have limited ability to investigate the wide variety of hormone treatments available notably the transdermal route of estrogen administration and progesterone. In addition, it is quite
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Cited by (13)
Metabolic transitions at menopause: In post-menopausal women the increase in serum uric acid correlates with abdominal adiposity as assessed by DXA
2013, MaturitasCitation Excerpt :This uricosuric effect might be set in the context of the multiple metabolic actions of endogenous E2 which most likely contributes to protecting women from cardiovascular and metabolic disorders during fertile life [28]. Indeed, several findings suggest that both endogenous and exogenous E2 (although the effectiveness of HRT on postmenopausal women CVD risk factors are still controversial [29]) contribute to decreasing the serum half-life of other cardiometabolic factors such as serum lipids (e.g. by increasing LDL hepatic receptors synthesis), pro-inflammatory cytokines and pro-oxidants species [30]. Thus, it might be speculated that the menopause-related decline of estrogens may deprive the female body of an important hypo-uricemic factor, and, consequently, favor the association between central adiposity and sUA level.
Effect of hormone replacement therapy in matrix metalloproteinase expression and intimal hyperplasia development after vascular injury
2013, Annals of Vascular SurgeryCitation Excerpt :Retrospective studies have recently challenged the long-standing hypothesis that estrogen might provide “vascular protection” for women, and many have demonstrated female gender itself as a predictor of adverse peripheral vascular outcomes.22,23 Many early studies established protective effects of HRT for vascular disease and other pathologies, and HRT became one of the most frequently prescribed medications in the USA.24 However, previous clinical studies by our group indicated that postmenopausal women taking HRT have worse outcomes after primary peripheral vascular intervention, including increased iliac angioplasty restenosis and decreased graft patency in infrainguinal bypass.3,4
The effects of pituitary and thyroid disorders on haemostasis: Potential clinical implications
2016, Clinical EndocrinologyChanges in hemostatic parameters after oral and transdermal hormone therapy in postmenopausal women
2011, Gynecological EndocrinologyVascular risks and HRT
2010, Revue du Praticien