雌激素的冠状动脉保护作用研究进展

雌激素的冠状动脉保护作用研究进展北京市潞河医院心内科潘国忠综述成都市第三人民医院心内科成都市心血管病研究所刘运德审校冠状动脉硬化性心脏病（ＣＨＤ）的发病率、死亡率存在着性别差异已是共识，但这种差异主要存在于绝经前的女性和同年龄段的男性之间，随着绝经后...     

第60例:临床表现胸痛、心电图异常、蛋白尿

正患者,女性,63岁,因"间断胸痛9个月"于2017年8月9日入院。患者9个月前无明显诱因出现胸痛,为刺痛,活动静息均发作,夜间亦发作,与呼吸及进食无关,胸痛有时持续数小时,发作无明确规律。分析患者老年女性,以胸痛为突出表现,发作诱因及规律不明确,常见胸痛原因考虑如下可能:(1)冠状动脉粥样硬化性心脏病:患者为绝经后女性,有冠状动脉粥样硬化的危险因素,需考虑冠状动脉粥样硬化性心脏病,但患者胸痛发作与     

不同民族女性冠心病发病规律及临床特点的研究进展

<正>冠状动脉粥样硬化性心脏病是指冠状动脉粥样硬化使血管腔狭窄或阻塞,或(和)因冠状动脉功能性改变导致心肌缺血缺氧或坏死而引起的心脏病,统称冠状动脉性心脏病(CHD),亦称缺血性心脏病[1]。随着人们生活水平的提高,心血管相关危险因素逐渐增加,女性心血管疾病的发病率和病死率也呈持续上升的趋势。许多相关研究已表明,CHD传统危险因素对不同民族CHD发病率、病死率的影响存在差异。我国是     

血清尿酸水平与冠状动脉粥样硬化性心脏病

冠状动脉粥样硬化性心脏病的危险因素众多,对于已明确的可控因素,应积极干预,对新的危险因素的探讨,有利于对冠状动脉粥样硬化性心脏病的早期干预治疗。该文对血清尿酸水平与血压、血糖、胰岛素抵抗、肥胖等冠状动脉粥样硬化性心脏病危险因素的关系及其是否为冠状动脉粥样硬化性心脏病的独立危险因素进行综述。     

雄激素与老年男性冠心病的关系

雄激素具有抗动脉粥样硬化的作用,补充生理剂量雄激素可改善老年男性的心肌缺血。雄激素对冠状动脉粥样硬化性心脏病的作用机制包括很多方面,雄激素可影响脂质代谢、血管张力、凝血纤维溶解系统、内皮细胞功能、血管壁平滑肌、巨噬细胞和雄激素受体及血栓烷A2受体。     

性别差异对肾素血管紧张素系统在冠心病发病中作用的影响

<正>冠状动脉粥样硬化性心脏病(冠心病)目前仍是危害人类健康的第一大疾病。人们通过长期临床实践观察到女性绝经前冠心病发病率低于同龄男性,绝经后这种差异消失[1]。探讨这种现象背后的原因一直是研究热点之一。肾素血管紧张素系统是人体内十分重要的体液调节系统。经典的肾素血管紧张素系统途径是指血管紧张素原(angiotensinogen,AGT)在肾素、血管紧张素转换酶(angio-     

心外膜脂肪组织与冠状动脉粥样硬化性心脏病关系及其机制的研究进展

目前认为,内脏脂肪组织堆积是冠状动脉粥样硬化性心脏病重要的危险因素。心外膜脂肪组织是内脏脂肪的一种类型,除了发挥代谢、产热和机械作用,还能分泌多种脂肪因子直接作用于邻近的冠状动脉,进而影响冠状动脉粥样硬化性心脏病进程。本文从解剖学、生理学、病理学、病理生理学和循证医学角度对心外膜脂肪组织与冠状动脉粥样硬化性心脏病关系及其机制的研究进展做一综述。     

冠心病患者的调脂治疗

冠状动脉粥样硬化性心脏病,简称冠心病,是指由于冠状动脉粥样硬化使管腔狭窄或阻塞导致心肌缺血、缺氧而引起的心脏病。本病多发生于40岁以上人群,男性多于女性。我国冠心病的发病率和死亡率正逐年上升。     

胰岛素抵抗在冠状动脉粥样硬化性心脏病中的作用及机制

胰岛素抵抗不仅导致胰岛素在促进葡萄糖摄取和利用方面受损,而且在冠状动脉粥样硬化性心脏病的发生和进展过程中起到至关重要的作用。部分冠状动脉粥样硬化性心脏病患者在发病前后出现了明显的胰岛素抵抗现象,治疗过程中降低患者体内的胰岛素抵抗水平能够改善其预后。近年来,越来越多的证据表明二者之间有着密切的联系。现就胰岛素抵抗在冠状动脉粥样硬化性心脏病中可能的作用和机制作一综述。     

激素替代治疗对绝经后女性血清血管紧张素转换酶活性的影响

血清血管紧张素转换酶(ACE)水平升高和男性冠状动脉粥样硬化性心脏病(CHD)发病危险升高相关。本文作者测定了绝经后女性接受激素替代治疗(HRT)之前和治疗期间的血清ACE活性水平,并与对照组进行比较。     

围绝经期妇女月经状况与心血管疾病的关系

目的：调查城市社区围绝经期女性中心血管疾病的患病率及其危险因素,并探讨绝经与心血管疾病危险因素之间的关系。方法采用现况调查的方法入选社区年龄40岁～59岁围绝经期妇女,填写调查问卷,内容包括：人口学特征、月经情况、身高体重、心血管疾病患病情况。根据月经状况将入选人群分为月经规律组、月经不规律组和绝经后期组。结果入选女性中,高血压和冠心病患病率分别为23.5%和7.7%,超重、肥胖、高脂血症及糖尿病的患病率分别为25.3%、2.4%、10.4%和6.2%,三组中绝经后期组超重、肥胖、高脂血症及其糖尿病比例最高。绝经后期组、月经不规律组及月经规律组中高血压的患病率分别为13.6%、5.8%和4.1%,具有统计学意义（P＆lt;0.01）。月经不规律组中冠心病患病率高于月经规律组（P＆lt;0.01）,月经不规律组中高脂血症患病率高于月经规律组（P＆lt;0.01）。结论高血压、高血脂、冠心病、肥胖和超重是城市社区围绝经期女性中最常见的心血管疾病。心血管疾病患病率及其危险因素从绝经过渡期即开始增加。     

Hormonal Therapy Increases Arterial Compliance in Postmenopausal Women

Objectives. This study investigated the effects of hormonal therapy on large arterial properties.Background. Arterial stiffness is an emerging risk marker for coronary heart disease and is potentially modifiable. Postmenopausal use of hormonal therapy is associated with a lower risk of coronary heart disease.Methods. Total systemic arterial compliance (SAC) and pulse wave velocity (PWV) were determined in 26 premenopausal and 52 postmenopausal women, 26 of whom were taking hormonal therapy.Results. Arterial compliance was greater in the premenopausal group (mean ± SEM 0.57 ± 0.04 arbitrary compliance units [ACU]) than in the postmenopausal group not taking hormonal therapy (0.26 ± 0.02 ACU, p = 0.001). Postmenopausal women taking hormonal therapy had a significantly increased total SAC compared with women not taking hormonal therapy (0.43 ± 0.02 vs. 0.26 ± 0.02 ACU, p = 0.001). PWV in the aortofemoral region in the premenopausal women was 6.0 ± 0.2 vs. 8.9 ± 0.3 m/s (p < 0.001) in untreated postmenopausal women. However, postmenopausal women taking hormonal therapy had a significantly lower PWV than those not taking hormonal therapy (7.9 ± 0.2 vs. 8.9 ± 0.3 m/s, p = 0.01). Eleven postmenopausal women had their hormone replacement therapy withdrawn for 4 weeks, resulting in a significant decrease in SAC and a significant increase in aortofemoral PWV.Conclusions. The increased SAC and decreased PWV in women receiving hormonal therapy suggest that such therapy may decrease stiffness of the aorta and large arteries in postmenopausal women, with potential benefit for age-related cardiovascular disorders. The reduction of arterial compliance with age appears to be altered with hormonal therapy.     

Hormone Replacement Therapy and Cardiovascular Risk

Hormone replacement therapy (HRT) is effective in suppressing postmenopausal symptoms and, in the past, many have claimed that it is cardioprotective. It was thought that the lower incidence of cardiovascular disease in premenopausal women was related to the cardioprotective effect of estrogen. Many of these studies were, however, observational studies. HRT alters many cardiovascular parameters, most beneficially. The mixed effect on these parameters make the overall result on cardiovascular risk difficult to predict. However, recent randomized, placebo-controlled trials have shown not only that HRT does not confer cardioprotection, but that it actually increases one's cardiovascular risk in the short term. Based on the current evidence, HRT should not be recommended in the hope that it will protect postmenopausal women against coronary heart disease.     

Modulation of coronary flow velocity reserve by gender, menstrual cycle and hormone replacement therapy

OBJECTIVES

The purpose of this study was twofold: 1) to examine the relationship between menstrual cycle and coronary flow velocity reserve (CFVR) in young healthy women, and 2) to evaluate the effect of hormone replacement therapy by estrogen on CFVR in postmenopausal women, using transthoracic color Doppler echocardiography (TTCDE).

BACKGROUND

Although the incidence of cardiovascular disease is lower in women before menopause compared with men, postmenopausal women have an incidence of coronary artery disease similar to that of men of the same age. This is mainly dependent upon estrogen deficiency. However, no clinical report has yet examined the effect of estrogen on CFVR, which is one index of coronary microcirculation.

METHODS

We examined 15 male and both 15 premenopausal and 10 postmenopausal female healthy volunteers. We measured coronary flow velocity of the left anterior descending coronary artery at baseline and hyperemic conditions during adenosine triphosphate infusion by TTCDE and determined CFVR. Each premenopausal woman was studied two times (menstrual [M] and follicular [F] phases) in one menstrual cycle. Fifteen men were also studied at a time corresponding to women’s menstrual cycle. The postmenopausal women were studied before and two hours after oral administration of conjugated estrogen (CE).

RESULTS

Serum 17β-estradiol level in premenopausal women increased in the F phase and decreased to the same levels as in men, as in the M phase and as in postmenopausal women (123 ± 9 pg/ml vs. 28 ± 6 pg/ml, 25 ± 9 pg/ml and 19 ± 11 pg/ml; p < 0.0001, respectively). The CFVR increased in the F phase compared with that in the M phase (4.8 ± 0.4 vs. 3.7 ± 0.8, p < 0.0001). We found that CFVR in men remained unchanged (3.7 ± 0.6 vs. 3.8 ± 0.5). After CE administration, CFVR increased compared with baseline in postmenopausal women (4.1 ± 0.8 vs. 3.4 ± 0.8, p < 0.005).

CONCLUSIONS

In premenopausal women, CFVR determined by TTCDE varied during the menstrual cycle, and in postmenopausal women, CFVR increased after acute estrogen replacement.     

Sex differences and the effects of sex hormones on hemostasis and vascular reactivity

Thrombus formation and vasospasm are involved in the initiation of acute ischemic events in the heart. Gender differences in persons with coronary artery disease and the incidence of myocardial ischemia have been clearly documented. In addition, it is well established that sex hormones influence the risk of developing coronary artery disease. Epidemiologic studies suggest that estrogen may exert a protective effect, yet the results of recently completed and ongoing prospective trials of estrogen and hormone (estrogen + progesterone) replacement suggest that these hormones can increase thrombotic events in postmenopausal women. This review focuses on sex (gender) differences in hemostasis and vascular reactivity and on the influence that sex hormones have on these physiologic systems. This review takes the novel approach of focusing on sex differences in hemostasis and vascular reactivity in healthy premenopausal women and men of a similar age. By comparing men and women in this age group, the confounding issues of age, pathology, or decline in sex hormone levels are avoided. Animal and in vitro investigations pertinent to examining potential cellular mechanism(s) of sex hormones in mediating these sex differences are discussed. We assume there is a relationship between the normal physiologic and pathologic effects of sex hormones; elucidating sex differences in normal cardiovascular function will help clarify the basis for sex differences in the incidence and manifestations of coronary heart disease and will aid in the future development of gender-specific therapies for cardiovascular disease.     

Sex steroids and plasma lipoprotein levels in healthy women: The importance of androgens in the estrogen-deficient state

The role of endogenous estrogens and androgens and their potential interaction in atherosclerosis is not well understood. Therefore, we investigated the effects of natural menopause and endogenous sex steroids on triglycerides (TG), a major risk factor for cardiovascular disease in women. Fasting lipid and lipoprotein concentrations, postheparin lipase activities, kinetic indicators of triglyceride lipolysis, and various hormone levels, including dehydroepiandrostenedione-sulfate (DHEA-S), (bioavailable) testosterone, and androstenedione, were determined in 18 premenopausal and 18 postmenopausal women, matched for age and body composition. Fasting plasma TG were 0.69 +/- 0.29 mmol/L in postmenopausal women and 0.73 +/- 0.33 mmol/L in premenopausal women (difference not significant [NS]). Approximately 30% of all plasma TG were present in the very-low-density lipoproteins (VLDLs) in both groups. No differences were found between groups in plasma lipolytic potential of TG-rich lipoproteins. Univariate analysis revealed that VLDL-TG concentrations were strongly related to insulin (r = 0.84, P =.0001) and androstenedione (r = 0.65, P =.004) in postmenopausal women. Multivariate analysis of potential determinants of VLDL-TG showed that insulin, androstenedione, and bioavailable testosterone were independent variables, explaining 87% of the variability (r = 0.93, P =.0001) in postmenopausal women. In contrast, in premenopausal women, the only identified predictor of fasting VLDL-TG in univariate and multivariate analysis was insulin (r = 0.72, P =.001). Our results show that the association of androgens with TG varied depending on androgen concentrations, the relative androgenic potential, and most importantly on hormonal milieu. Endogenous androgens were only related to plasma VLDL-TG in the estrogen-deficient state.     

Endogenous testosterone and endothelial function in postmenopausal women

OBJECTIVE: It is well known that coronary heart disease incidence increases in women after menopause. This phenomenon was related to reduced levels of female sex hormones. Estrogen decline, however, is not the only hormonal change during the postmenopausal period and estrogen administration did not protect women from cardiovascular disease. Therefore, it is justified to explore other hormonal changes. The role of androgens is still controversial. The aim of the present study was to investigate the relationship between endogenous sex hormones and endothelial function, measuring the brachial artery flow-mediated dilation. METHODS AND RESULTS: Sixty postmenopausal women were consecutively enrolled and underwent a clinical and biochemical examination. Brachial artery flow-mediated dilation was also evaluated by ultrasound. After correction for confounding variables, testosterone was positively correlated to flow-mediated dilation (beta=0.277, P=0.03). Indeed, women in the lowest testosterone tertile had a flow-mediated dilation smaller than that in the highest tertile (P=0.02). CONCLUSIONS: This result could suggest that the development of cardiovascular disease after menopause is due not only to estrogen decline but also to androgen decline. More studies are needed to evaluate the role of androgen replacement therapy on postmenopausal women with low level of this hormone.     

Coronary heart disease risk reduction in postmenopausal women: the role of statin therapy and hormone replacement therapy

The incidence of coronary heart disease in women rises sharply in the years following menopause, and prescribing of hormone replacement therapy in the belief that it might compensate for the loss of estrogen-mediated cardioprotection is widespread. However, controlled trials have failed to show a beneficial effect of hormone replacement therapy on the incidence of coronary events, and recent evidence suggests that hormone replacement therapy may even have a deleterious effect on primary coronary heart disease prevention. Statins are recommended as first-line treatment for lowering low-density lipoprotein cholesterol levels in women and are extremely valuable in reducing coronary heart disease risk in this group. An awareness of the benefits of appropriate statin treatment, and evidence showing that they can be safely added to hormone replacement therapy prescribed for the relief of menopausal symptoms and osteoporosis, provides the opportunity to optimize clinical outcomes for coronary heart disease among the large and expanding population of postmenopausal women.     

Role of hormone-replacement therapy for prevention of coronary artery disease in women

The postmenopausal increase in the incidence of coronary artery disease implied a protective effect of estrogens. Nonrandomized, clinical and experimental studies have supported this notion. In the first randomized study (HERS 1998) no protective effect on prognosis of postmenopausal women with coronary artery disease was demonstrated. Also, in healthy postmenopausal women no beneficial effect of a hormone-replacement therapy on coronary events was shown (WHI-Study 2002, 2004). Therefore, hormone-replacement therapy is not recommended for prophylaxis of cardiovascular disease in healthy women or in women with documented coronary artery disease (Recommendation class I, evidence-level A). The continuation or the start of a hormone- replacement therapy is only justified for therapy of severe menopausal symptoms. Women should be informed that changes in lifestyle including not smoking, a heart healthy diet, and regular exercise are the most important measures to prevent cardiovascular diseases.