The effect of hormone replacement therapy on arterial distensibility and compliance in perimenopausal women: a 2-year randomised trial

Westendorp, I. C. D.; Kleijn, Miriam J.J. de; Bots, Michiel L.; Bak, Annette; Planellas, Juan; Bennink, Herjan J.T. Coelingh; Hofman, Albert; Grobbee, Diederick E.; Witteman, J.C.M.

doi:10.1016/s0021-9150(99)00438-4

Cited by 27 publications

(18 citation statements)

References 54 publications

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“…In addition, several reports could not identify any increases in arterial compliance in women receiving estrogen and progesterone [113,114]. These results suggest that progesterone may counteract the effects of estrogen on arterial elasticity.…”

Section: Progesteronementioning

confidence: 79%

Gender differences in artery wall biomechanical properties throughout life

Rossi

Francès

Kingwell

et al. 2011

Journal of Hypertension

114

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Elevated large artery stiffness and pulse pressure have emerged as important risk factors for cardiovascular disease. The genders differ in large artery biomechanical properties throughout the lifespan with females displaying higher stiffness than males during the prepubertal years and a dramatic increase after menopause. Males on the other hand experience an increase in arterial stiffness postpuberty and a linear increase thereafter, suggesting that females have intrinsically stiffer large arteries than males, but that such effects are mitigated by sex steroids during the reproductive years. This review discusses anthropometric and sex steroid influences on gender differences in large artery stiffness and pressure dynamics from childhood to senescence. In particular, the sex-specific effects of estrogen, progesterone and testosterone on vascular structure and function and how these influence arterial stiffness are explored. These factors may contribute in part to the observed gender differences in the pathophysiology and clinical manifestations of cardiovascular disease.

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Section: Progesteronementioning

confidence: 79%

Gender differences in artery wall biomechanical properties throughout life

Rossi

Francès

Kingwell

et al. 2011

Journal of Hypertension

114

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“…31 Large artery distensibility decreases after menopause, 32 but small, short-term studies in relatively healthy, postmenopausal women suggest HRT use may attenuate arterial stiffness. 15,16 This effect may vary by formulation of HRT and be limited to certain subgroups of women.…”

Section: Discussionmentioning

confidence: 99%

Pulse Pressure and Coronary Atherosclerosis Progression in Postmenopausal Women

et al. 2005

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Abstract-Pulse pressure, an index of large artery stiffness, has been associated with coronary events. However, mechanisms for this association remain unclear. In this study, we examined the relationship between pulse pressure and the progression of coronary atherosclerosis and the effects of hormone replacement therapy (HRT) on pulse pressure in postmenopausal women with angiographically confirmed coronary disease followed for 3.2 years in the Estrogen Replacement in Atherosclerosis (ERA) trial. In the ERA trial, 309 postmenopausal women (mean age 66Ϯ7 years) with coronary disease were randomized to estrogen, estrogen plus progestin, or placebo, and followed for 3.2 years. Ten standardized epicardial segments were measured for minimal diameter values at baseline and follow-up using quantitative coronary angiography. For this study, mixed-model analysis of covariance was used to: (1) test the association between pulse pressure and change in mean minimum diameter (MMD) adjusted for baseline MMD and (2) the effect of HRT on follow-up pulse pressure. After adjustment for potential confounders, there was a significant graded increase in progression of coronary stenosis with increasing quartiles of baseline pulse pressure (P test for trendϭ0.0001). The progression rate in women with the highest quartile of baseline pulse pressure was 5-fold higher than in women in the lowest quartile (PϽ0.01). In postmenopausal women with coronary disease, increased levels of baseline pulse pressure are associated with subsequent progression of coronary atherosclerosis in postmenopausal women. HRT had no detectable effect on pulse pressure. Key Words: pulse Ⅲ atherosclerosis Ⅲ women P ulse pressure, an index of large artery stiffness, 1 is a significant predictor of coronary artery disease outcomes, including myocardial infarction 2-5 and restenosis after percutaneous coronary intervention. 6 However, the mechanisms underlying this association remain to be elucidated. In animal models, increased aortic stiffness is associated with coronary ischemia 7 and progression of coronary atherosclerosis. 8 In clinical studies, increased pulse pressure (PP) has been associated with atherosclerosis progression in the aorta 9,10 and carotid arteries, 11-14 but its relationship to coronary atherosclerosis progression in humans remains unknown.Any association between PP and coronary atherosclerosis progression in women may be confounded by hormonal status. Studies in healthy postmenopausal women suggest hormone replacement therapy (HRT) use may have favorable effects on large artery compliance. [15][16][17][18] However, these effects may be limited to specific formulations of HRT 17,19 or certain subgroups of women. 19 Furthermore, aging, established atherosclerosis, 20 or concomitant progestin use 21 may attenuate some of the favorable effects of estrogen on vasculature. Additional studies are needed to examine the association of PP with coronary atherosclerosis progression in postmenopausal women and assess the impact of HRT use on PP.In this stu...

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Section: Discussionmentioning

confidence: 99%

“…It is of interest to note that the reported beneficial effects of hormone replacement therapy appear to be related to early "perimenopausal" treatments, and the effectiveness of this therapy significantly diminishes if it is not initiated until later in menopause. 20,21 Alternatively, the lessened responsiveness in older SHR may reflect an impairment of their estrogen response mechanisms, eg, reduced estrogen receptors.The results of this study suggest that the mechanisms that underlie NaCl-sensitive hypertension in female middle-aged SHR are, at least in some respects, similar to the mechanisms that underlie NaCl-sensitive hypertension in young male SHR. In young male SHR, the ability of a high NaCl diet to increase arterial pressure is dependent on the sympathetic nervous system.…”

mentioning

confidence: 99%

Estrogen Depletion Increases Blood Pressure and Hypothalamic Norepinephrine in Middle-Aged Spontaneously Hypertensive Rats

et al. 2003

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Abstract-In male spontaneously hypertensive rats (SHR) a high NaCl diet increases arterial pressure via a reduction in anterior hypothalamic nucleus norepinephrine release. Young female SHR are relatively well protected from this NaCl-sensitive hypertension, but depletion of both endogenous and dietary estrogens greatly exacerbates NaCl-sensitive hypertension. This study tests the hypothesis that estrogen also protects late middle-aged female SHR from NaCl-sensitive hypertension and that this effect is mediated by an estrogen-related effect on hypothalamic norepinephrine release. Ten-month-old female SHR were ovariectomized and placed on a phytoestrogen-free diet containing either basal or high NaCl. Each rat was implanted with a silastic tube containing 17␤ estradiol or vehicle. Three months later, arterial pressure and hypothalamic norepinephrine metabolite levels (MOPEG) were measured. On the basal NaCl diet, estrogen-depleted rats displayed increased arterial pressure (12 mm Hg) and decreased anterior hypothalamic nucleus MOPEG (20%). Both effects were reversed by estrogen treatment. In all groups, the high NaCl diet increased arterial pressure by over 35 mm Hg and reduced anterior hypothalamic nucleus MOPEG by Ͼ60%. Across all groups, there was a significant inverse correlation between arterial pressure and anterior hypothalamic nucleus MOPEG. These data suggest that both dietary NaCl excess and estrogen depletion raise arterial pressure in middle-aged female SHR by a decreasing hypothalamic norepinephrine. Key Words: estrogen Ⅲ norepinephrine Ⅲ sodium Ⅲ sympathetic nervous system Ⅲ blood pressure H ypertension significantly contributes to premature death in the fastest-growing segment of the population, ie, adults over 65 years of age. 1 The incidence of hypertension in this age group is about 60%. [2][3][4] Further, between 30% and 50% of hypertensive patients are NaCl-sensitive, ie, they display a significant (Ͼ10%) increase in blood pressure when placed on a high NaCl diet (200 to 250 mEq Na ϩ /d for 7 days). The NaCl-sensitive hypertensive patients, in contrast to normotensive and NaCl-resistant hypertensive subjects, fail to suppress plasma norepinephrine (NE) after the ingestion of a diet high in NaCl. 5,6 These and other studies suggest that the sympathetic nervous system contributes importantly to NaCl-sensitive hypertension in aging humans. 7,8 Several lines of evidence indicate that, compared with men, premenopausal women have a lower rate of hypertension. After menopause this relative protection appears to be lost, and women experience a rapid rise in hypertension (including salt-sensitive hypertension). 9,10 This increase appears to be related to the menopausal loss of estrogen. Our studies in spontaneously hypertensive rats (SHR) demonstrate that young female SHR (compared with age-matched male SHR) have a lower arterial pressure and a reduced hypertensive response to excess dietary NaCl. 11 Elimination of most endogenous estrogen by ovariectomy causes no significant change in arterial pressur...

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The effect of hormone replacement therapy on arterial distensibility and compliance in perimenopausal women: a 2-year randomised trial

Cited by 27 publications

References 54 publications

Gender differences in artery wall biomechanical properties throughout life

Gender differences in artery wall biomechanical properties throughout life

Pulse Pressure and Coronary Atherosclerosis Progression in Postmenopausal Women

Estrogen Depletion Increases Blood Pressure and Hypothalamic Norepinephrine in Middle-Aged Spontaneously Hypertensive Rats

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