放疗引起的心血管疾病

放疗引起的心血管疾病,通常无症状,影响着心血管系统的每个构成部分。心包损伤是最常见的并发症,可表现为心包积液、缩窄性心包炎等,放疗损伤还可影响心肌、瓣膜、传导系统、周围血管系统等。一旦出现,临床症状,并发症的致死率将显著增加。随着肺癌、乳腺癌、霍奇金病等患病率增高,放疗引起的心血管疾病发病率将随之增长,如何鉴别和评估放疗引起的心血管并发症就显得至关重要,如何治疗和预防也将是心脏病学和肿瘤学专家共同面临的难题。     

糖尿病合并心血管疾病的治疗

糖尿病合并心血管疾病的治疗山东省立医院（２５００２１）王爱红，张虹，邵建华糖尿病患者合并心血管疾病后，其病死率较非糖尿病者明显增高。男性及女性糖尿病患者死于心血管并发症者，分别比非糖尿病患者高２倍和５倍。这主要与其胰岛素缺乏或相对不足，引起糖、脂肪、...     

阿司匹林对心血管疾病一级预防作用

心血管疾病是人类的主要死因，尤其是老年人致死、致残的重要疾病。预防心血管疾病的发生是减少其对我国大众健康及生命危害最重要的手段。心血管病的预防可分为一级、二级和三级预防。一级预防主要是降低心血管疾病的发生率，尤其是存在心血管发生的     

尿毒症性心血管疾病研究新进展

本文综述近年对尿毒症性心血管疾病的有关研究进展，重点阐述透析相关的低血压，左心室肥厚，左心室收缩功能异常，心律失常和心力衰竭等问题。     

探索心血管疾病安全而有效的康复训练

目的：探索心脏监测和康复训练在老年心血管疾病康复中的价值。方法：本组利用Ｈｏｌｔｅｒ和＾２０１Ｔｌ心肌显像对６６例病人进行心脏监测和对１５例冠心病人进行监测下的康复训练,结果：７８．５％（Ｈｏｌｔｅｒ）～９４．２％（＾２０１Ｔｌ）患存在无症状性心肌缺血现象,尤６０岁以上患明显,采用适宜的训练项目、强度,未见加重心肌缺血现象。结论：心脏监测有利于康复训练安全进行,康复训练时不能主必意强求达到“靶     

心血管疾病患者安全拔牙的临床探讨

目的：探讨对心血管疾病患者安全拔牙措施。方法：回顾性分析66例心血管疾病患者拔牙的资料。结果：本组66例心血管病患者拔牙均顺利成功，仅4例术中出现心率加快．暂时血压升高．经对症处理后症状消失,其他均无副作用。结论：心血管疾病患者的拔牙在术前充分准备。术中充分麻醉、准确操作和观察下是安全的，并发症是可以避免的。     

糖尿病并发心血管疾病的机理研究进展

心血管疾病 (CVDs)是糖尿病常见的并发症和主要死因。糖尿病并发CVDs的主要危险因素包括 :高血压、肥胖、动脉粥样硬化、脂质代谢失常、微蛋白尿、内皮功能失常、血小板高凝聚性、凝血 血纤溶系统活性失常以及糖尿病心肌病等。本文简要综述了糖尿病患者脂质代谢异常、内皮功能失常、蛋白质非酶糖化、氧化应激等病理生理生化变化促使动脉粥样硬化形成和CVDs发生的分子机理。     

如何改善慢性肾衰竭患者心血管疾病的预后

心血管疾病是终末期肾脏病 (ＥＳＲＤ)患者最常见的并发症。ＥＳＲＤ患者心血管疾病的病死率是一般人群的 16 6～ 17 7倍。据美国肾脏病资料系统(ＵＳＲＤＳ) 1999年统计 ,由心血管疾病所致的死亡占ＥＳＲＤ总病死率的 4 5 %。我国ＥＳＲＤ的原发病因和年龄分布与西方国家有很大差异 ,但同年中华肾脏病学会公布的肾脏透析移植登记报告表明 ,ＥＳＲＤ患者由心血管疾病所致的病死率亦高达 5 0 %。因此 ,心血管疾病已成为影响ＥＳＲＤ患者生存率和致残率的最为重要的因素。ＥＳＲＤ患者心血管疾病的发生率较一般人群高5～ 10倍 ,尽管导致心血…     

肥胖体型高血压病与心血管疾病并发症的关系

本文对612例高血压病患者的临床资料进行回顾性分析研究.按体重指数分肥胖型与非肥胖型二组,分析其在心血管疾病并发症及危险因素等方面的差异,以便为高血压病预后及心血管病危险因素防治提供依据.     

Ghrelin and cardiovascular diseases

Ghrelin, a newly discovered bioactive peptide, is a natural endogenous ligand of the growth hormone (GH) secretagogue receptor and initially identified as a strong stimulant for the release of GH. Subsequent research has shown that ghrelin and its various receptors are ubiquitous in many other organs and tissues. Moreover, they participate in the regulation of appetite, energy, bodyweight, metabolism of glucose and fat, as well as modulation of gastrointestinal, cardiovascular, pulmonary, immune functions and cell proliferation/apoptosis. Increasing evidence has demonstrated that ghrelin has a close relationship with cardiovascular system. Ghrelin and its receptors are widely distributed in cardiovascular tissues, and there is no doubt that the effects of ghrelin in the cardiovascular system are mediated not only via its growth-hormone-releasing effect but also by its direct effects on the heart. Exogenous administration of ghrelin can dilate peripheral blood vessels, constrict coronary artery, improve endothelial function, as well as inhibit myocardial cell apoptosis. So, ghrelin may have cardiovascular protective effect, including lowering of blood pressure, regulation of atherosclerosis, and protection from ischemia/reperfusion injury as well as improving the prognosis of myocardial infarction and heart failure. Some of these new functions of ghrelin may provide new potential therapeutic opportunities for ghrelin in cardiovascular medicine. In this paper, we will review the existing evidence for cardiovascular effects of ghrelin, including the cardiovascular function, the variations in ghrelin plasma levels in pathophysiologicalogical conditions, the possible protective mechanisms of ghrelin, as well as its future potential therapeutic roles.     

Urotensin-II and cardiovascular diseases

Urotensin-II (U-II) is a vasoactive factor with pleiotropic effects. U-II exerts its activity by binding to a G-protein-coupled receptor termed UT. U-II and its receptor are highly expressed in the cardiovascular system. Increased U-II plasma levels have been reported in patients with cardiovascular disease of varying etiologies. We and others have shown that U-II and UT expression is elevated in both clinical and experimental heart failure and atherosclerosis. U-II induces cardiac fibrosis by increasing fibroblast collagen synthesis. In addition, U-II induces cardiomyocyte hypertrophy and increased vascular smooth muscle cell proliferation. We have shown that U-II antagonism using a selective U-II blocker, SB-611812, attenuates cardiac dysfunction by decreasing cardiomyocyte hypertrophy and cardiac fibrosis. We have also shown that SB-611812 reduces neointimal thickening and increases lumen diameter in a rat restenosis model of carotid artery angioplasty. These findings suggest an important role for U-II in cardiovascular dysfunction and remodeling.     

促红细胞生成素在心血管疾病中的应用

促红细胞生成素原用于贫血的治疗,但近年研究发现除促造血作用以外,还有细胞保护及促血管生成等作用,可用于缺血性心脏病、心力衰竭等心血管疾病的治疗.本文就其在心血管疾病中的应用进展情况作一综述.     

Women and cardiovascular diseases

The authors draw attention to the important role played by menopause in the onset of arterial hypertension, enhanced coronary risk and dyslipidemia, for which a particularly useful association has been found to be estrogens, only if administered by mouth (alone or with progestins), and statins. The authors review numerous studies for or against the use of estrogens as a means of reducing arterial hypertension and the incidence of myocardial ischemia in menopausal women. In order to ensure therapeutic efficacy, replacement estrogen therapy should not be started at not too late an age, but instead as young as possible (the first 5 years after the start of menopause are optimal), namely before levels of endothelial estrogen receptors start to fall. Moreover, therapy should not be continued for more than 5 years in order to avoid the risk of breast cancer and endometrial carcinoma. With regard to myocardial infarction, it is worth noting that women show a higher frequency of silent and atypical infarction leading to a late diagnosis and therefore the arrival in the coronary unit half an hour or an hour later than men. Together with the onset of myocardial infarction at an older age in women compared to men (5-10 years), and the fact that diagnosis is less accurate in women and treatment less sophisticated, this accounts for the higher immediate and medium-term mortality figures in women following myocardial infarction. However, at least in America studies have shown that the less aggressive diagnostic and therapeutic management of myocardial infarction in women compared to men is not sufficient to cause a significant difference in mortality between men and women 30 days after the event. Turning to arrhythmia, it is worth recalling that supraventricular tachycardia with close rapid complexes, caused by return in the atrioventricular node is more frequent in females and in the second lutein or progestin phase of the menstrual cycle, thus demonstrating the protective role of estrogens against the onset of arrhythmia. The authors also point out the frequent association between ischemic ictus and chronic non-valvular atrial fibrillation in women aged over 75 since they present a very high risk (94%) of death by ischemic ictus. On the one hand, the guidelines recommend the use of anticoagulating therapy in these patients, but on the other there is a very high risk of hemorrhage which acts as a major constraint. Lastly, pregnancy is mentioned as a condition that facilitates the onset of arrhythmia; for example, orthodromic supraventricular tachycardia in Wolf Parkinson White and ventricular tachycardia which usually regresses post-partum.     

Ghrelin and cardiovascular diseases

In 1999, a peptide from the stomach called ghrelin was discovered, which exerts potent growth hormone releasing powers. Subsequent studies revealed that it exerts a potent orexigenic action. In addition, the beneficial effects of ghrelin in cardiovascular diseases have been recently suggested. In humans as well as in animals, administration of ghrelin improves cardiac function and remodeling in chronic heart failure. In an animal model for myocardial infarction, ghrelin treatment early after coronary ligation effectively reduces fatal arrhythmia and, consequently, mortality, suggesting the potential therapeutic role of the peptide in acute myocardial infarction. Although how ghrelin may influence the cardiovascular system is not fully understood, the cardiovascular beneficial effects are mediated possibly through a combination of various actions, such as an increase in growth hormone level, an improvement in energy balance, direct actions to the cardiovascular cells, and regulation of the autonomic nervous activity. Of note, current experimental evidence suggests that ghrelin may act centrally to decrease sympathetic nervous system activity through peripheral afferent nerve. Thus, administration of ghrelin might become a unique new therapy for cardiovascular diseases.