Effects of estrogen replacement on plasma lipoproteins and apolipoproteins in postmenopausal, dyslipidemic women.

The effects of oral estrogen replacement (ethinyl estradiol 0.02 mg/d) on plasma triglyceride, total cholesterol, very-low-density lipoprotein (VLDL) cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and apolipoprotein (apo) A-I and B levels and LDL particle size were assessed in 20 postmenopausal women with a previous hysterectomy and various forms of dyslipidemia (LDL cholesterol > or = 4.14 mmol/L [160 mg/dL] and/or HDL cholesterol < or = 1.03 mmol/L [40 mg/dL]). All subjects were studied while on a standard cholesterol-lowering diet, and were sampled in the fasting state before beginning estrogen therapy and after a mean of 13 weeks of estrogen therapy. Lipids were measured by standardized enzymatic techniques, apos were measured by enzyme-linked immunoassays, and LDL particle size was measured by gradient gel electrophoresis. Mean values for plasma lipid parameters (mmol/L) at baseline and during estrogen replacement were as follows: triglyceride, 2.11 and 2.75 (30% increase); total cholesterol, 7.45 and 6.52 (13% decrease); VLDL cholesterol, 1.09 and 1.22 (12% increase); LDL cholesterol, 5.09 and 3.70 (27% decrease); and HDL cholesterol, 1.27 and 1.58 (24% increase). Mean values for apo A-I were 163 and 254 mg/dL (56% increase), and for apo B they were 170 and 148 mg/dL (13% decrease). The LDL particle score was 4.09 and 4.52 (11% smaller). Changes in all parameters were statistically significant (P = .05) except for VLDL cholesterol. These data indicate that estrogen replacement is effective in decreasing LDL cholesterol and apo B concentrations and increasing HDL cholesterol and apo A-I concentrations in dyslipidemic postmenopausal women, but it should not be used in patients with baseline fasting triglyceride levels higher than 2.82 mmol/L (250 mg/dL) unless it is accompanied by a progestin. Our data indicate that this form of estrogen replacement could lower the risk of coronary artery disease (CAD) by more than 50% in these women, based on favorable alterations in plasma lipoproteins.     

Combined hormone replacement therapy improves endothelial function in healthy postmenopausal women

OBJECTIVES: Large scale epidemiological studies suggest that hormone replacement therapy (HRT) reduces cardiovascular events in postmenopausal women. Improvement in endothelial function may contribute to this protective effect. DESIGN: In a prospective, double blind study, 61 healthy postmenopausal women were randomized to receive either oral continuous combined HRT [oestradiol 2 mg and norethisterone acetate (NETA) 1 mg per day] or placebo. Endothelial function, assessed by flow-mediated vasodilation (FMD) of the brachial artery and expression of soluble endothelial cell adhesion molecules (CAM) were determined before, after 3 and 6 months of therapy. RESULTS: The FMD was significantly improved in women on combined HRT (from 5.97% to 10.94% after 3 months and to 10.58% after 6 months; both P < 0.01 versus baseline values) and did not change in the placebo group (6.92% at baseline, 5.86% after 3 and 6.26% after 6 months). After 3 months of combined HRT, significant decreases of 24.6% for E-selectin and 13.9% for intercellular adhesion molecule-1 (ICAM-1) were observed (both P < 0.01 versus baseline values) and were sustained after 6 months of therapy, whilst no differences emerged in the placebo group. CONCLUSIONS: Oestradiol and norethisterone acetate improve endothelial function by both enhancing FMD and reducing the levels of soluble E-selectin and ICAM-1 in healthy postmenopausal women.     

雌激素替代治疗对妇女冠心病患者血浆一氧化氮和内皮素的影响

目的 :研究绝经后妇女冠心病 ( CHD)患者血浆一氧化氮 ( NO)和内皮素 ( ET- 1)之间的关系 ,探讨雌激素替代治疗 ( ERT)改善血管内皮功能的作用机制。方法 :5 8例绝经后 CHD患者随机分为治疗组和安慰剂组。治疗组每天给予克龄蒙 (含戊酸雌二醇 2 mg,第 1～ 12天服 ;含戊酸雌二醇 2 m g和醋酸环丙孕酮 1m g,第 13～ 2 2天服 ) 1片 ,安慰剂组每天给予安慰剂 1片 ,观察治疗 6个月后血浆 NO和 ET- 1的变化。结果 :治疗组血浆 NO水平显著升高 ( P <0 .0 1) ,ET- 1显著降低 ( P <0 .0 1) ,NO与 ET- 1的比率亦显著升高 ( P <0 .0 1) ,安慰剂组则变化不明显。结论 :ERT能改善绝经后妇女 CHD患者 NO与 ET- 1的比率 ,这可能是其改善血管内皮功能的机制之一 ,可能有助于绝经后妇女 CHD的 2级预防     

Effect of estrogen-progestin replacement therapy on plasma lipids and lipoproteins in postmenopausal women

Serum levels of cholesterol (Chol), triglycerides (TG), low-density lipoprotein cholesterol (LDL) high-density lipoprotein cholesterol (HDL), both apolipoproteins A1 and B (Apo A1, Apo B), follicle-stimulating hormone (FSH) luteinizing hormone (LH), estradiol (E2), progesterone (P), testosterone (T) and steroid hormone binding globulin (SHBG) were measured in postmenopausal women, before and after four different estrogen-progestin replacement therapies. Each woman was her own control to avoid genetic or socioeconomic differences. Our results showed that serum E2 and TG significantly increased and serum FSH, LH, LDH, Apo B, and Chol significantly decreased after all treatments. Serum P and T did not significantly change after any of the treatments. HDL, Apo A1 and SHBG significantly increased in the groups treated with medroxiprogesterone acetate (MPA) but not in the group treated with Norgestrel. We conclude that estrogen-progestin replacement therapy in postmenopausal women leads to profound and beneficial changes in plasma lipids and lipoproteins and that treatments with cyclic or continuous MPA could provide greater protection against coronary heart disease (CHD).     

雌激素对绝经后妇女冠心病治疗作用的观察

目的探索雌激素对绝经后妇女冠心病的防治机制及疗效。方法将１０８例绝经１年以上的女性冠心病患者随机分为三组（各３６例），甲组口服结合雌激素（倍美力）０．６２５ｍｇ１／ｄ，乙组口服７甲基异炔诺酮（利维爱）２．５ｍｇ１／ｄ，丙组口服安慰剂１片１／ｄ，于服药前及服药后第３、６个月末检测血脂谱及ＥＣＧ，并记录心绞痛发作情况。结果倍美力治疗后可使胆固醇（ＴＣ）降低１２．８％，甘油三酯（ＴＧ）降低１７．０％，低密度脂蛋白胆固醇（ＬＤＬＣ）降低２９．０％，高密度脂蛋白胆固醇（ＨＤＬＣ）上升１４６％。利维爱治疗后ＴＣ降低８．７％，ＴＧ降低１５．６～３３．８％、ＨＤＬＣ降低１９．７～２８．３％（Ｐ值均＜００１），ＬＤＬＣ无显著变化。倍美力及利维爱治疗第３、６个月后对心绞痛症状的总有效率分别为９０９％、９３５％和８３．３％和９３．１％，对ＥＣＧ缺血性改变的总有效率分别为７６．７％、８２．１％和７８．６％、８１４％，两种药物对妇女冠心病的心肌缺血疗效差异无显著性（Ｐ＞０．０５）。结论雌激素替代治疗可显著改善绝经后妇女冠心病患者的异常血脂及心肌缺血     

Long-term estrogen replacement therapy is associated with improved exercise capacity in postmenopausal women without known coronary artery disease

BACKGROUND: Short-term estrogen administration improves vasodilation and has been shown to improve exercise capacity. However, it is unknown whether long-term estrogen replacement therapy is associated with improved exercise capacity in postmenopausal women without known coronary artery disease. METHODS AND RESULTS: We studied 248 postmenopausal women without known coronary artery disease (mean age 63.5 years); 158 (64%) were current or past hormone replacement therapy (HRT) users and 108 (44%) were current users of HRT. Attributes potentially affecting exercise capacity and cardiac risk factors were carefully measured. These included duration of estrogen replacement therapy, all variables in the Framingham risk index, physical activity level, body mass index, waist-to-hip ratio, presence of osteoporosis, and family history of heart disease. We measured maximal oxygen uptake (MVO (2)) and anaerobic threshold as objective markers of exercise capacity. The relation between exercise capacity and use of HRT was analyzed with the use of logistic regression, controlling for confounding variables. We found that fitness, as measured by MVO (2) and anaerobic threshold, was significantly greater in women who had used HRT currently or in the past compared with women who had never used HRT. This difference in fitness was not confounded by age or physical activity level. CONCLUSIONS: Estrogen replacement therapy is associated with increased exercise capacity as measured by MVO (2) and anaerobic threshold in postmenopausal women without coronary artery disease. This finding is consistent with the beneficial effect of short-term estrogen administration on improved endothelium-dependent and endothelium-independent vasodilation.     

Effects of estrogen replacement therapy on serum lipid values and angiographically defined coronary artery disease in postmenopausal women.

To examine the effects of estrogen replacement on lipids and angiographically defined coronary artery disease (CAD) in postmenopausal women, lipid profiles were obtained in 90 consecutive postmenopausal women undergoing diagnostic coronary angiography. Eighteen women (20%) were receiving estrogen and 72 (80%) were not. CAD (defined as greater than or equal to 25% luminal diameter narrowing in a major coronary artery) was present in only 22% of women (4 of 18) receiving estrogen and in 68% (49 of 72) who were not (p less than 0.001), with an odds ratio of 0.13. Mean high-density lipoprotein (HDL) cholesterol level was significantly higher (63 +/- 6 vs 48 +/- 2; p less than 0.01) and mean total/HDL cholesterol ratio significantly lower in women receiving estrogen than in those who were not (4.2 +/- 0.5 vs 5.1 +/- 0.2; p less than 0.05). The other lipid values were similar in both groups. On multiple logistic regression analysis, absence of estrogen use was the most powerful independent predictor of the presence of CAD (p less than 0.001), with total/HDL cholesterol ratio as the only other variable selected (p less than 0.01). Thus, among 90 consecutive postmenopausal women undergoing diagnostic coronary angiography, estrogen replacement therapy was associated with an 87% reduction in the prevalence of CAD, and those receiving estrogen had a significantly higher mean HDL cholesterol level and lower mean total/HDL cholesterol ratio.     

雌激素替代治疗对绝经后妇女冠心病血糖、血脂等的影响

目的：探讨雌激素对血糖、血胰岛素及血脂的影响。方法：对绝经后女性冠心病（CHD）60例，正常对照组30例做75g糖耐量试验，测空腹、餐后1．2小时血糖，血胰岛素（INS）及血脂（ISI），计算胰岛素敏感指数。CHD 组给予利维受（每片含7－甲异炔诺酮2.5mg）治疗12周，然后重复上述各项目检测。结果：与对照组相比，CHD组血糖、INS及ISI均有显性差异（P＜0．001）。利维爱治疗后，血糖、INS、总胆固醇、低密度脂蛋白胆固醇、载脂蛋白B较治疗前降低，而ISI、高密度脂蛋白胆固醇、载脂蛋白A水平升高，治疗前、后有显性差异（P＜0．001）。结论：雌激素替代治疗可以降低绝经后CHD患的血糖、INS水平，降低胰岛素抵抗（IR），纠正脂质代谢紊乱。     

Estrogen replacement and coronary artery disease. Effect on survival in postmenopausal women

The relationship among postmenopausal estrogen use, coronary stenosis, and survival was examined retrospectively in 2268 women undergoing coronary angiography. The patients were selected for study if their age was 55 years or older at the time of angiography or if they had previously undergone bilateral oophorectomy. Postmenopausal estrogen use in 1178 patients with coronary artery disease (greater than 70% stenosis) and 644 patients with mild to moderate coronary artery disease (5% to 69% stenosis) was compared with 446 control subjects (0% stenosis) using life-table analysis. Over 10 years of follow-up, there was no significant difference in survival among patients initially free of coronary lesions on arteriography who had either never used (377) or ever used (69) estrogens. Among patients with mild to moderate coronary stenosis, 10-year survival of those who had never used estrogens was 85.0% and it was 95.6% among 99 "ever users." Survival was 60.0% among those with more than 70% coronary stenosis who had never used estrogen and it was 97.0% among 70 ever users. The "never users" group were older (65 vs 59 years), had a lower proportion of cigarette smokers (40% vs 57.1%), a higher proportion of subjects with diabetes (21.7% vs 12.9%) and hyperlipidemia (58% vs 44%), and approximately equal numbers of hypertensives (56.0% vs 54.3%). Cox's proportional hazards model was used to estimate survival as a function of multiple covariables. Estrogen use was found to have a significant, independent effect on survival in women. We conclude that estrogen replacement after menopause prolongs survival when coronary artery disease is present, but it has less effect in the absence of coronary artery disease.     

The effect of hormone replacement therapy alone and in combination with simvastatin on plasma lipids of hypercholesterolemic postmenopausal women with coronary artery disease

Objectives. This study sought to compare hormone replacement therapy (HRT), simvastatin and their combination in the management of hypercholesterolemia in postmenopausal women with coronary artery disease (CAD).Background. Lipid-lowering therapy reduces mortality in hypercholesterolemic women with CAD. In postmenopausal women HRT seems to increase survival, particularly those with ischemic heart disease, and this is partly due to changes in lipid levels.Methods. We studied 16 postmenopausal women with CAD and fasting total cholesterol <200 mg/dl and low-density lipoprotein (LDL) cholesterol <130 mg/dl. We compared HRT (0.625 mg of conjugated estrogen and 2.5 mg of medroxyprogesterone acetate daily) with simvastatin (20 mg daily) and their combination in a randomized, crossover, placebo-controlled study. Each treatment period was 8 weeks long with a 4-week washout interval between treatments.Results. Simvastatin, HRT and their combination significantly reduced total and LDL cholesterol by 35%, 13%, and 33% and 45%, 20%, and 46%, respectively, compared to placebo (p < 0.001). However, simvastatin and the combination was superior to HRT (p < 0.001), and none of our patients had total cholesterol <180 mg/dl and LDL cholesterol <100 mg/dl on HRT alone. High-density lipoprotein cholesterol was not significantly affected by any of the active treatments, and triglycerides were lower during simvastatin therapy compared to placebo (p < 0.01). Apolipoprotein B was significantly reduced by simvastatin, alone and combined with HRT, by 39% and 35%, respectively, compared to placebo (p < 0.001). Alone and in combination with simvastatin, HRT significantly increased apolipoprotein A-I by 11% and 12%, respectively, compared to placebo (p < 0.05) and decreased lipoprotein (a) by 23% and 33%, respectively, compared to placebo (p < 0.05), whereas simvastatin had no significant effect on either of these parameters.Conclusions. In hypercholesterolemic postmenopausal women with CAD, HRT exerts beneficial effects on plasma lipids but the levels currently recommended for secondary prevention are not achieved. Hormone replacement therapy combined with simvastatin is well tolerated and extremely effective, as the two therapies seem to be additive.     

雌激素替代治疗对绝经后女性血脂代谢及血浆内皮素的影响

目的 探讨雌激素替代治疗(ERT)对绝经妇女血脂及血浆内皮素的影响。方法 选择自然停经妇女60例,其中30例用ERT,另30例用安慰剂治疗30天。治疗前后均检测促卵泡激素(FSH)、雌二醇(E_2)、孕酮(P)、睾酮(T)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)及血浆内皮素-1(ET-1)。结果 ERT组妇女血清E_2水平较治疗前明显升高,P、T水平无明显变化,TC、TG及LDL-C下降,HDL-C升高,ET-1水平显著下降;安慰剂组妇女上述指标均无显著变化。线性相关分析显示:绝经妇女E_2与TC、TG、LDL-C及ET-1负相关,与HDL-C正相关;TC与ET-1明显正相关。结论 ERT能改善绝经妇女血脂代谢和降低其血浆内皮素-1水平。两者相互促进和补充,从而发挥心血管保护作用。     

雌激素替代疗法对绝经后冠心病患者及正常妇女的影响

目的观察雌激素治疗绝经后冠心病患及正常妇女体内血脂、血小板聚集率、氧自由基及纤溶活性变化。方法选５３例绝经后妇女冠心病患为冠心病组,４２例绝经后健康妇女为正常对照组,每组病例再单盲随机分为治疗组和安慰剂组,治疗组予尼尔雌醇（每月４ｍｇ／次）治疗６个月,安慰剂组予安慰剂治疗,观察治疗前后患雌激素水平及血脂各项指标、血小板聚集率、氧自由基和纤溶活性变化。结果冠心病组雌激素水平低于正常对照组（Ｐ＜     

Blood pressure control and hormone replacement therapy in postmenopausal women at risk for coronary heart disease

Background Coronary heart disease (CHD) in women is strongly associated with estrogen deprivation. For example, risk for CHD increases dramatically after menopause. However, the role of hormone replacement therapy (HRT) in CHD prevention currently is unresolved. To better understand CHD in women, the precise mechanisms by which estrogen affects circulatory function require clarification. Evidence suggests that exogenous estrogen may affect blood pressure (BP) control, but its interaction with other CHD risk factors has not been systematically characterized. The present study examines the role of mildly elevated resting BP, family history of CHD, and HRT on BP responses to stress in postmenopausal women. Methods Postmenopausal women on long-term HRT were recruited along with a control group of postmenopausal women not on HRT. These women were divided into higher versus lower risk for CHD on the basis of resting BP and family history of CHD. BP control mechanisms were assessed before, during, and after a computer-controlled laboratory stressor. Results Results indicate that women with elevated resting BP and positive family history of CHD have exaggerated BP reactivity to stress and that HRT inhibits this effect. Conclusions This study suggests that unmedicated postmenopausal women with mildly elevated resting BP and positive family history of CHD have altered BP control as indicated by exaggerated BP responses to stress. HRT eliminates the cumulative effect of resting BP and family history on BP reactivity, suggesting that the circulatory effects of estrogen replacement may operate, at least in part, through normalization of BP reactivity in higher-risk postmenopausal women. (Am Heart J 2002;143:711-7.)     

Effect of diet and exercise intervention on inflammatory and adhesion molecules in postmenopausal women on hormone replacement therapy and at risk for coronary artery disease

Inflammation and the recruitment of monocytes into the artery wall are thought to be important aspects in the initiation and progression of atherosclerosis. The present study was designed to examine the effects of a rigorous diet and exercise intervention on plasma lipids and inflammatory and circulating adhesion molecules. Twenty postmenopausal women at risk for coronary artery disease (CAD) were placed on a high-fiber, low-fat diet, where food was provided ad libitum and daily aerobic exercise, primarily walking, was performed. In each subject, pre- and post-intervention fasting blood was drawn for serum lipid, insulin, glucose, C-reactive protein (CRP), serum amyloid A (SAA), interleukin-6 (IL-6) and both soluble (s) intracellular and vascular adhesion molecule (sICAM-1 and sVCAM-1) were measured. After 2 weeks, significant reductions in body mass index (BMI) (P <.001), glucose (P <.05), insulin (P <.01), all serum lipids, and total cholesterol (total-C):high-density lipoprotein-cholesterol (HDL-C) (P <.01). Reductions in homeostasis model assessment for insulin resistance (HOMA-IR) (P <.01), CRP (P <.01), SAA (P <.01) and sICAM-1 (P <.05) were noted, as well as an increase in the quantitative insulin sensitivity check index (P <.05). Reductions were also noted in 5 women not using hormone replacement therapy (HRT). No significant reductions were found in IL-6 or sVCAM-1 in response to the intervention. Overall, this intervention resulted in improved metabolic and lipid profiles, reduced inflammatory, and cell adhesion molecules in postmenopausal women in the absence of caloric restriction. The rapid improvements may reduce the risk of acute myocardial infarction (MI), and if sustained, these changes may mitigate the risk for atherosclerosis progression and its clinical consequences.     

Effect of sulfasalazine on inflammation and endothelial function in patients with established coronary artery disease

Inflammation is critical for atherosclerosis development and may be a target for risk-reduction therapy. In experimental studies, activation of the inflammatory regulator, nuclear factor kappa B (NFlB), contributes to endothelial activation and reduced nitric oxide production. We treated patients with coronary artery disease with sulfasalazine, an inhibitor of NFκB, and placebo in a randomized, double-blind, crossover study design. Brachial artery flow-mediated dilation (FMD) and digital vascular function were measured at baseline and after each 6-week treatment period. Of the 53 patients enrolled in the crossover study, 32 (age 60 ± 10, 22% female) completed all the visits, with a high rate of study withdrawal due to gastrointestinal side effects. In a subset of 10 participants, we compared the effects of 4 days of sulfasalazine treatment (n = 5) to no treatment (n = 5) on NFκB-regulated gene expression in peripheral blood mononuclear cells. Tumor necrosis factor α-stimulated expression of CD69 and NFlB subunit p50 was significantly blunted after 4 days of sulfasalazine treatment but not after no treatment. However, FMD and digital vasodilator response did not significantly change from baseline with long-term sulfasalazine treatment. Short-term sulfasalazine inhibited NFlB activity; however, long-term treatment was poorly tolerated and did not improve endothelial function. Our findings suggest that sulfasalazine therapy is not the optimal anti-inflammatory treatment for reversing endothelial dysfunction in cardiovascular disease. Further studies are warranted to investigate the potential for NFlB inhibition to reduce cardiovascular risk.     

雌激素替代治疗对绝经后妇女冠心病者血脂代谢及抗氧化作用的研究

对32例绝经后妇女（PMW）冠心病患者（CHD组）进行雌激素替代治疗（ERT），以观察对其血脂代谢及机体抗氧化水平的影响。另选取绝经后健康妇女30例为对照组。CHD组口服尼尔雌醇（CEE3）每月2次，每次2mg，连用6个月，分别于用药前、用药后3个月及6个月检测总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL－C）、低密度脂蛋白胆固醇（LDL－C）、脂蛋白（a）［LP（a）］、氧化修饰低密度脂蛋白（Ox－LDL）、丙二醛（MDA）及超氧化物歧化酶（SOD）。结果表明ERT前CHD组与对照组比较LP（a）、Ox－LDL及MDA水平明显升高（P＜0．05），而SOD总活力显著降低；CHD组于ERT后TC无明显变化，TG呈升高趋势（P＞0.05），而LDL-C、TC／HDL－C和LDL－C／HDL－C显著下降（P＜0．01），LP（a）也明显降低（P＜0．05），而HDL－C显著上升（P＜0．01）；血浆Ox－LDL、血清MDA显著下降（P＜0．01），血清SOD总活力明显上升（P＜0．05），提示ERT不仅能显著改善PMW之CHD患者血脂紊乱，而且能有效地提高机体抗氧化水平。     

Effect of hormone replacement therapy on age-related increase in carotid artery intima-media thickness in postmenopausal women

The aim of this study was to determine the changes in carotid artery intima-media thickness as measured by B-mode ultrasound in postmenopausal women receiving hormone replacement therapy (HRT) or not. One hundred and fifty-nine healthy postmenopausal women aged 45-65 years were recruited from our menopause clinic. All the selected women were free of cardio-vascular diseases and had no cardio-vascular risk factors. None of the women were receiving lipid-lowering or antihypertensive drugs. Because carotid artery intima-media thickness was shown to be strongly and positively correlated with age in women aged 55 years and older but not before, women were divided into four groups according to age (<55 vs. > or =55 years) and use of HRT (current users vs. never users). All the treated women received non-oral 17beta-estradiol with a non-androgenic progestin and had started HRT within the first year after menopause. Scanning of the right common carotid artery was performed with a B-mode ultrasound imager and thickness of the intima-media complex as well as luminal diameter of the artery were determined using an automated computerized procedure. Within each age group (i.e. <55 or > or =55 years), women had comparable demographic characteristics and only differed by HRT use. Long-term treated women had significantly lower total cholesterol levels than untreated women (P=0.005). Triglycerides, low-density lipids (LDL)-cholesterol and high-density lipids (HDL)-cholesterol levels, systolic and diastolic blood pressure were not significantly different between users and non-users. In women <55 years, no significant difference in carotid intima-media thickness was found between current users (mean 2.5+/-1.4 years) and non users. In older women, the mean values of carotid intima-media thickness were significantly smaller in current users (mean 6.9+/-3.3 years) than in never treated women: 0.50+/-0.05 versus 0.56+/-0.07 mm, P<0.0001. Carotid artery intima-media thickness was significantly correlated to age in never users (r=0.5, P<0.0001) but not in women who were currently receiving HRT (r=0.2, ns). These findings suggest an apparent protective effect of long-term HRT on age-related thickening of the intima-media of the right common carotid artery. This may contribute to explain the apparent cardio-protective effect of HRT after the menopause.