Carotid artery wall thickness in women treated with hormone replacement therapy (original) (raw)

Hormone Replacement Therapy and Intima-Media Thickness of the Common Carotid Artery

Stroke, 1999

Background and Purpose —Observational data suggest that hormone replacement therapy (HRT) reduces morbidity and mortality from cardiovascular disease in healthy postmenopausal women. The mechanisms underlying this protection are not entirely clear but may include inhibition of the atherosclerotic process. Methods —We studied the association between ever use of HRT and intima-media thickness (IMT) of the common carotid artery in 1103 naturally menopausal women, aged 55 to 80 years, in the Rotterdam Study, a community-based cohort study in a suburban area of Rotterdam, Netherlands. Mean and maximum IMT of the common carotid artery were measured noninvasively with B-mode ultrasound. Results —Ever use of HRT for ≥1 year was associated with a decreased mean and maximum IMT compared with never users (mean IMT, 0.719 mm [SE 0.01] versus 0.742 mm [SE 0.004], P =0.03; maximum IMT, 0.952 mm [SE 0.015] versus 0.983 mm [SE 0.006], P =0.04), after adjustment for age, smoking, educational level, ...

Hormone replacement therapy use is associated with a lower occurrence of carotid atherosclerotic plaques but not with intima-media thickness progression among postmenopausal women. The vascular aging (EVA) study

Atherosclerosis, 2003

Background: Information on the impact of hormone replacement therapy (HRT) on carotid atherosclerosis is limited. Moreover, transdermal estrogens have not been investigated. Methods: We examined association of HRT use with ultrasonographically assessed carotid atherosclerotic plaque occurrence and mean common carotid artery intima-media thickness (CCA Á/IMT) progression. Within the Vascular Aging (EVA) Study, a community-based cohort, 815 postmenopausal women aged 59 Á/71 have been followed during 4 years. Among these women, 166 had already used HRT. Results: Women who had ever used HRT experienced a lower occurrence of plaques (8.6 versus 19.1%, P0/0.003). After adjustment for the main cardiovascular risk factors, odds-ratio for plaque occurrence was 0.41 (95% confidence interval 0.21 Á/0.78, P0/0.01) among ever users of HRT compared with never users. When transdermal route of estrogen administration was used, adjusted odds-ratio was 0.66 (95% confidence interval 0.47 Á/0.99, P 0/0.04). The progression of IMT, which was measured at a plaque-free site and adjusted on initial levels of CCA Á/IMT did not differ between ever and never users of HRT. It was 0.011 mm per year among ever users and 0.012 mm per year among never users (P0/0.61). Conclusion: These data suggest that HRT use may prevent the development of atherosclerotic plaques in postmenopausal women, especially when estrogens are administered by transdermal route. #

Hormone replacement therapy and distensibility of carotid arteries in postmenopausal women: a randomized, controlled trial

Journal of the American College of Cardiology, 2000

The study objective was to clarify in a randomized, controlled, observer-blind trial whether hormone replacement therapy (HRT) improves elastic properties of the common carotid artery in women with signs of subclinical atherosclerosis, especially in subgroups with increased risk, and whether less progestin enhances the effect. BACKGROUND Previous observational studies have yielded conflicting results on the influence of HRT on central arteries. Some studies reported improvement of distensibility by estrogen alone or in the subgroup of smokers. METHODS A total of 321 postmenopausal women were randomized to 1 mg 17␤-estradiol plus 0.025 mg gestodene for 12 days every month (HRT 1), or 1 mg 17␤-estradiol plus 0.025 mg gestodene for 12 days every third month (HRT 2), or no-HRT, during 48 weeks. In 173 women, distensibility of the common carotid artery was determined before and after therapy by M-mode ultrasound and brachial blood pressure measurement. RESULTS Change of distensibility was small and similar in the three treatment groups. In the subgroup of current smokers, HRT 2 (low progestin) increased distensibility by 32% (HRT 2: 8.2 Ϯ 11.7; HRT 1: 0.6 Ϯ 6.0; no HRT: Ϫ1.8 Ϯ 6.8 ϫ 10 Ϫ3 /kPa, p ϭ 0.025 for no-HRT vs. HRT 2). In the subgroups with elevated blood pressure, high low density lipoprotein (LDL) cholesterol, or high age, no effect of HRT was detected. CONCLUSIONS This randomized intervention study demonstrates that long-term HRT with estrogen and progestin does not substantially influence distensibility of central arteries. Yet, in currently smoking postmenopausal women, HRT with low progestin seems to improve distensibility; this merits further study in a specifically designed trial.

Hormone replacement therapy in perimenopausal women and 2-year change of carotid intima-media thickness

Maturitas, 1999

In a 2-year longitudinal, calcium-controlled study we evaluated bone density and metabolism in perimenopausal women with initial ovarian failure, and the effects of hormone replacement with a low dose oral contraceptive preparation (OC). In perimenopausal oligomenorrhoic women (n = 16) a significant (P < 0.01) increase in cycle length and plasma FSH levels as well as a parallel decrease in plasma estradiol levels (P < 0.01) were evident. In this group, despite the calcium supplementation (500 mg/day), a significant (P < 0.001) increase in the biochemical markers of bone remodelling paralleled a significant (P < 0.001) decrease (-3.4% after 24 months) in bone density. Conversely, in premenopausal oligomenorrhoic women treated with a low dose oral contraceptive (CC) formulation (30 mcg ethinyl estradiol plus 75 mcg gestodene, n = 16), bone markers showed a significant (P < 0.01) decrease, that paralleled a slight but significant (P < 0.01) increase (+ 1.71%) in bone density. These data suggest that premenopausal administration of OC can prevent the acceleration of bone turnover and reverse the decrease in bone density that follows the premenopausal impairment of ovarian function.

Effect of Oral Postmenopausal Hormone Replacement on Progression of Atherosclerosis : A Randomized, Controlled Trial

Arteriosclerosis, Thrombosis, and Vascular Biology, 2001

Postmenopausal hormone replacement therapy (HRT) is associated with low cardiovascular morbidity and mortality in epidemiological studies. Yet, no randomized trial has examined whether HRT is effective for prevention of coronary heart disease (CHD) in women with increased risk. The objective of this study was to determine whether HRT can slow progression of atherosclerosis, measured as intima-media thickness (IMT) in carotid arteries. Carotid IMT is an appropriate intermediate end point to investigate clinically relevant effects on atherogenesis. This randomized, controlled, observer-blind, clinical, single-center trial enrolled 321 healthy postmenopausal women with increased IMT in Ն1 segment of the carotid arteries. For a period of 48 weeks, subjects received either 1 mg/d 17␤-estradiol continuously plus 0.025 mg gestodene for 12 days every month (standard-progestin group), or 1 mg 17␤-estradiol plus 0.025 mg gestodene for 12 days every third month (low-progestin group), or no HRT. Maximum IMT in 6 carotid artery segments (common, bifurcation, and internal, both sides) was measured by B-mode ultrasound before and after intervention. HRT did not slow IMT progression in carotid arteries. Mean maximum IMT in the carotid arteries increased by 0.02Ϯ0.05 mm in the no HRT group and by 0.03Ϯ0.05 and 0.03Ϯ0.05 mm, respectively, in the HRT groups (PϾ0.2). HRT significantly decreased LDL cholesterol, fibrinogen, and follicle-stimulating hormone. In conclusion, 1 year of HRT was not effective in slowing progression of subclinical atherosclerosis in postmenopausal women at increased risk.

Effect of postmenopausal hormone replacement on atherosclerosis in femoral arteries

Maturitas, 2002

Objecti6es: On the basis of epidemiological and experimental data, it has been supposed that hormone replacement therapy (HRT) inhibits atherosclerosis in postmenopausal women. This randomized controlled trial examined whether 1 mg 17b-estradiol daily, combined cyclically with 0.025 mg gestodene in every month (HRT 1), or in every third month (HRT 2) slows the increase of intima-media thickness in femoral arteries compared with no HRT. Methods: Healthy postmenopausal women (n=321) with an increased risk for future vascular disease as indicated by \ 1 mm of intima-media thickness in the carotid arteries were equally randomized to one of the three groups for 48 weeks. Ultrasound scans of femoral arteries were recorded at study start and study end, together with a thorough clinical examination and laboratory work-up. Results: Complete scans were obtained in 260 of the 264 subjects who participated until study end. Mean maximum intima-media thickness of four femoral artery segments (common and superficial, both sides) was 0.93 90.37 mm (mean 9S.D.) at study start. It increased by 0.02 9 0.05, 0.02 9 0.05, and 0.039 0.05 mm in the HRT 1, HRT 2 and no HRT groups, respectively (HRT 1 versus no HRT, HRT 2 versus no HRT; both P\ 0.2). Compared with no HRT, HRT significantly lowered follicle stimulating hormone, low-density lipoprotein cholesterol, and fibrinogen. Conclusions: In this 1-year trial, irrespective of the progestogen dose used, HRT with 1 mg 17b-estradiol did not inhibit progression of femoral artery atheroslerosis in postmenopausal women with subclinical vascular disease.

Association of menopause and hormone replacement therapy with large artery remodeling

Fertility and Sterility, 2011

Objective: To evaluate the remodeling of large arteries according to age at menopause, duration of menopause, and use of hormone therapy (HT). Design: A cross-sectional study consisting of baseline measurements of a multicentric randomized trial were used to evaluate arterial parameters. Setting: The study was conducted in France, Belgium, and the Netherlands in academic hospitals and private clinics. Patient(s): Postmenopausal women (n ¼ 538) with mild hypercholesterolemia. Intervention(s): None. Main Outcome Measure(s): Common carotid artery intima-media thickness (CCA-IMT), central pulse pressure, and aortic stiffness (carotid-femoral pulse wave velocity) were measured and centrally controlled for quality. Multivariate regression analysis was used to assess the possible covariates associated with arterial parameters. Result(s): Women were 58 AE 6 (mean AE SD) years of age with an age of 50 AE 5 at menopause and a mean duration of menopause of 8 AE 7 years. Lower age at menopause, time since menopause, and absence of HT use were independently associated with worsening of the arterial parameters. After multivariate analysis, HT was associated with a lower CCA-IMT (À40 mm [range À64 to À1]), whereas lower age at menopause and menopause duration were respectively associated with a CCA-IMT increase (25 mm/5 y and 27 mm/5 y). Similarly, values of central pulse pressure and pulse wave velocity were lower in HT users (À3.1 mm Hg [À5.1 to À0.9] and À0.31 m/s [À0.63 to À0.02], respectively) but worsened with age at menopause and menopause duration. Conclusion(s): The age at menopause, the time since menopause, and the use of HT are independently associated with the thickening and stiffening of the large arteries.

Hormone Replacement Therapy Is Associated with Less Coronary Atherosclerosis in Postmenopausal Women

2010

Most observational studies indicate that hormone replace- ment therapy (HRT) protects women from cardiovascular dis- ease. Two recent randomized trials, however, showed no re- duction in coronary events with HRT in postmenopausal women. A randomized study evaluating subclinical athero- sclerosis showed a beneficial effect of estrogen. In the current study we evaluated the association between HRT and coro- nary artery