血管紧张II受体阻滞剂—Losartan作用及其临床应用

血管紧素ＩＩ（ＡＮＧＩＩ）是肾素－血管紧张素系统（ＲＡＳ）中重要的介质，它使用于特异性受体，导致血管收缩和醛固酮的释放。Ｌｏｓａｒｔａｎ是一种口服有效，代谢稳定，具有选择性的ＡＮＧＩＩ受体阻滞剂。它具有血管扩张效应，有防止容量超负荷引起心肌厚及左室扩大的作用，增加冠流量，与卡托普利，依那普利等ＡＣＥＩ相比，Ｌｏｓａｒｔａｎ的作用时间长，不良反应少，耐受性好，临床上是一种新的，高效能的治疗高血压和充     

血管紧张素受体阻滞剂在心力衰竭治疗中的作用及地位

充血性心力衰竭(congestive heart failure,CHF)是各种心脏病终末发展的一种结局,由心肌梗死或其他心血管疾病等多种因素引起,具有很高的致残率及病死率.各个阶段心力衰竭患者的健康和生活质量都受到很大影响,随着病情进展,患者的生存期明显缩短.因此,对心力衰竭的防治已成为近年来临床心脏病学家关注和研究的热点.     

联用β受体阻滞剂和血管紧张素转换酶抑制剂对扩张型心肌病预后的影响

目的观察长期联合应用β受体阻滞剂和血管紧张素转换酶抑制剂(ACEI)对扩张型心肌病预后的影响.方法按就诊顺序将患者随机分为A、B组,A组33例给予β受体阻滞剂和ACEI加常规治疗,B组39例常规治疗,平均服药38.2±12.6月,随访1年和3年的临床和实验资料.结果A组的病死率明显低于B组,且A组在心肌重塑修复、心功能改善、神经内分泌激素水平和减少室性心律失常的发生等方面亦明显优于B组.结论扩张型心肌病患者长期联合应用β受体阻滞剂和ACEI制剂可明显逆转心肌重塑、改善心功能和预后.     

血管紧张素抑制剂还是受体阻滞剂?

医生很喜欢用新的药物取代旧的药物,即使旧的药物完全胜任有余。对于新的血管紧张素受体阻滞剂（简称ARB）和旧的血管紧张素抑制剂（简称A—CEI）。情况也是如此。这两种药物都是常用的降压药,作用于同一目标——血管紧张素,只是作用的途径不一样。     

血管紧张素受体阻滞剂的临床药理学

血管紧张素转换酶抑制剂 (ａｎｇｉｏｔｅｎｓｉｎ ｃｏｎｖｅｒｔ ｉｎｇｅｎｚｙｍｅｉｎｈｉｂｉｔｏｒ ,ＡＣＥＩ)在临床上应用已近 2 0年 ,其主要作用是通过抑制血管紧张素转换酶 (ａｎ ｇｉｏｔｅｎｓｉｎ ｃｏｎｖｅｒｔｉｎｇｅｎｚｙｍｅ ,ＡＣＥ) ,减少肾素 血管紧张素系统 (ｒｅｎｉｎ ａｎｇｉｏｔｅｎｓｉｎｓｙｓｔｅｍ ,ＲＡＳ)中的主要活性物质血管紧张素Ⅱ (ａｎｇｉｏｔｅｎｓｉｎⅡ ,ＡｎｇⅡ ) ,使血压下降 ,并产生一系列有益的神经内分泌效应 ,其临床疗效已为许多大规模前瞻性随机、双盲、对照临床试验所证实。这类制…     

扩张型心肌病大鼠胶原重塑与血管紧张素II及其I型受体变化

目的　探讨血管紧张素II及其I型受体在扩张型心肌病心室间质胶原重塑中的作用。方法　用呋喃唑酮饲养Wistar大鼠建立扩张型心肌病大鼠模型 ,超声心动图检测大鼠心功能 ,病理学测量大鼠左室内径和左游离壁厚度 ,HE和VG染色分别观察大鼠心肌细胞和间质胶原纤维的变化 ,免疫组化检测血管紧张素Ⅱ及其I型受体表达水平。结果　扩张型心肌病大鼠左室收缩功能下降 ;左心室内径增大、游离壁变薄 ;心肌细胞肥大、变性 ,核增大、分裂、畸形 ,间质胶原纤维增生 ;左室心肌血管紧张素II表达水平升高 ,而血管紧张素III型受体表达水平降低。结论　血管紧张素II水平升高可能是呋喃唑酮扩张型心肌病大鼠心室间纤维化的原因之一。     

血管紧张素转化酶抑制剂与血管紧张素受体阻滞剂治疗充血性心力衰竭效果对比

目的：研究分析对充血性心力衰竭患者采用血管紧张素受体阻滞剂和血管紧张素转化酶抑制剂治疗的效果,为其临床治疗和应用提供有效的理论依据。方法本次研究的开展时间为2013年1月-2014年1月,均为该阶段在本院接受治疗的充血性心力衰竭患者共208例,根据患者临床期间所接受的不同用药方案,将其随机分为两组,对照组患者104例,临床期间采用贝那普利片（血管紧张素转化酶抑制剂）治疗,观察组患者104例,临床期间采用缬沙坦片（血管紧张素受体阻滞剂）治疗,比较两组患者的治疗效果,研究中所涉及的数据采用 SPSS 统计软件进行分析处理。结果本研究中,观察组患者的治疗有效率为96.15％,对照组患者的治疗有效率为82.69％,观察组明显高于对照组,两组比较差异明显,具有统计学意义,P〈0.05。结论在充血性心力衰竭的治疗中,采用血管紧张素受体阻滞剂治疗的效果更佳,在临床治疗中应加以重视。     

血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂联合治疗糖尿病肾病的临床研究

目的比较血管紧张素转换酶抑制剂（ACEI）和血管紧张素受体阻滞剂（ARB）单独及联合治疗糖尿病肾病（DN）的疗效。方法183例DN患者，随机分为三组，分别予贝那普利、洛沙坦或两药联合治疗12周。比较治疗前后血压、尿蛋白及血钾和血Cr等的变化。结果上述两药均能有效降低DN的血压和尿蛋白且作用相似；联合治疗的降尿蛋白作用更明显（P〈0．05），但二者的降压效果相似（P〉0．05）。治疗前后的血钾、血Cr和Ccr无明显变化（P〉0．05）。结论对于DiN患者，ACEI和ARB联合治疗与单药相比具有更强的降尿蛋白作用，且这种作用是通过独立于血压的机制实现的。     

Apical Hypertrophic Cardiomyopathy in an Adolescent

To our knowledge, this is one of the few reported cases of apical hypertrophic cardiomyopathy in an adolescent patient in the United States. We describe a clinical presentation of an adolescent male who presented for cardiac evaluation and was found to have an apical variant of hypertrophic cardiomyopathy.     

Hypertrophic Cardiomyopathy in a Neonate Associated with Nemaline Myopathy

Nemaline myopathy is a congenital nonprogressive skeletal muscle disorder with a characteristic rod body formation in the skeletal muscle fibers. Cardiac involvement in nemaline myopathy is rare, although both dilated and hypertrophic cardiomyopathy have been reported. We describe an infant diagnosed with hypertrophic cardiomyopathy and hypotonia on the first day of life. Muscle biopsy confirmed nemaline myopathy at 3 weeks of age. The diagnosis of nemaline myopathy precluded consideration of heart transplantation, thus shifting the focus to comfort care. This is the earliest presentation of hypertrophic cardiomyopathy reported in the literature in the setting of nemaline myopathy. The approach to determining an etiology for hypertrophic cardiomyopathy in an infant is reviewed.     

线粒体DNA变异与肥厚型心肌病

目的肥厚型心肌病（hypertrophiccardiomyopathy,HCM）是指未伴心室扩张的不明原因左室肥厚,以室间隔非对称性肥厚常见。HCM多由编码肌小节蛋白的基因突变所致;有少部分患者由线粒体DNA突变引起,呈母系遗传。线粒体DNA变异导致HCM的分子机制可能与引起的线粒体结构功能改变,造成氧化磷酸化缺陷,ATP合成不足。本文着重对与HCM相关的mtDNA变异位点作一综述。     

Survival Implications: Hypertrophic Cardiomyopathy in Noonan Syndrome

Objectives. To understand relationships and survival implications between structural heart disease and hypertrophic cardiomyopathy in Noonan syndrome (Noonan syndrome‐HCM), we reviewed the clinical course of 138 children with Noonan syndrome diagnosed with cardiovascular abnormalities and compared survival with the 30 children with Noonan syndrome‐HCM with 120 contemporaneous children with nonsyndromic HCM. Methods. Study cohorts represent consecutive cases diagnosed at our institution 1966 through 2006. Outcomes were modeled using multiphase parametric techniques followed by multivariable regression with bagging. Results. Cardiac abnormalities in Noonan syndrome: Cardiac abnormalities in the 138 Noonan syndrome children included pulmonary valve dysplasia (52%), hypertrophic cardiomyopathy (22%), atrial septal defect (20%), ventricular septal defect (10%), mitral valve dysplasia (6%), coarctation (3%), and Fallot's tetralogy (2%). Need for surgery was high but not different from children with structural defects coexisting with HCM. Overall, late survival in children with Noonan syndrome and cardiac defects was good (91 ± 3% at 15 years), although significantly worse for those with Noonan syndrome‐HCM (P < .01). Noonan syndrome‐HCM vs. nonsyndromic HCM: In the 30 children with Noonan syndrome‐HCM, structural cardiac malformations coexisted in 18 (57%). The incidence of structural cardiac malformations in nonsyndromic HCM was instead 3/120 (2.5%, P < .001). Risk‐adjusted late survival was significantly worse for Noonan syndrome‐HCM than for nonsyndromic HCM (P= .02). Conclusions. Noonan syndrome‐HCM frequently coexists with structural cardiac malformations, whereas nonsyndromic HCM does not; their natural histories may therefore be different. Late survival is significantly worse for Noonan syndrome‐HCM than nonsyndromic HCM.     

Cardioprotective Effect of Enalapril in Renovascular and Angiotensin II Hypertension

The influence of chronic treatment with enalapril or losartan (10 or 30mg/kg/24h, respectively) on cardiac mass was evaluated in one-kidney, one clip (1K-1C) hypertensive rats submitted to sodium restriction 3 weeks after clipping and in rats infused for 10 days with angiotensin II (ANGII: 200ng/kg/min). In 1K-1C hypertension, cardiac mass and arterial pressure were reduced to a similar extent by enalapril and losartan. In ANGII hypertension, enalapril and losartan blunted the increase in cardiac mass whereas losartan but not enalapril prevented the development of hypertension. The cardioprotective effect of enalapril was attenuated by concomitant blockade of bradykinin receptors (Hoe 140: 300pg/kg/24h) in both models. The beneficial influence of enalapril on cardiac mass appears to be independent of its effect on blood pressure and ANGII generation and seems partly mediated by endogenous bradykinin in these high ANGII models of hypertension.     

Hypertrophic Cardiomyopathy: Infants,Children, and Adolescents

Hypertrophic cardiomyopathy (HCM) is characterized by inappropriate left ventricular hypertrophy (LVH) in the setting of a nondilated left ventricle. HCM is often associated with asymmetric LVH, a family history of HCM, sarcomeric genetic mutations, and an increased risk of sudden cardiac death. There is a wide clinical variability in HCM presenting during childhood and a relative lack of data on the pediatric population. This review will cover HCM presenting in infancy, childhood, and adolescence.