氯沙坦对老年高血压左室肥厚及血管紧张素Ⅱ影响的临床观察

目的：观察氯沙坦对老年高血压左室肥厚及血管紧张素Ⅱ。方法：选择43例老年高血压伴左室肥厚病人,给予氯沙坦50～mg/d共12～17个月的治疗,分别测定治疗前后左室重量指数（LVMI）、左室功能及血浆血管紧张素Ⅱ的水平。结果：与治疗前相比,LVMI明显减少,而血管紧张素Ⅱ浓度有增加的趋势,但无统计学意义（P＞0．05）。结论：氯沙坦在有效降压的同时可逆转左室肥厚,改善左室功能的作用,尤以舒张功能为著。     

氯沙坦或氨氯地平对老年高血压左室肥厚伴阵发性房颤的影响

目的 通过观察老年高血压左室肥厚患者心脏结构及功能的改变与阵发房颤的变化。探讨氯沙坦对老年高血压左室肥厚伴阵发房颤的影响。方法 选择83例老年高血压左室肥厚患者，随机分为二组：氯沙坦组43例。口服氯沙坦50-100mg／天；氨氯地平组加例，口服氨氯地平5—10mmg／d，治疗12-17个月。分别测定治疗前后阵发房颤的变化及左房内径与左室结构及功能的变化。结果 与治疗前比，氯沙坦组及氨氯地平组左室重量指数（LVM1）均明显减少（均P〈0.05），E／A较治疗前增加，即等容舒张时间较治疗前缩短（均P〈0．05）。说明左室舒张功能均得到改善，左房内径较治疗前减小（均P〈0．05），动态心电图中阵发房颤较治疗前减少（78．5％、14．3％）。结论 氯沙坦在有效降压的同时，既可有效改善左房的结构重构及电重构，又可逆转左室肥厚，改善左室舒张功能，降低左房压力，减小左房内径，减少阵发房颤的发生。     

氯沙坦逆转老年高血压左室肥厚的疗效观察

目的：观察血管紧张素Ⅱ受体拮抗剂氯沙坦逆转老年高血压左室肥厚的疗效。方法：40例老年高血压患口服氯沙坦50mg,1次／日,共6个月。治疗前、后分别行多普勒声心动图检查。结果：治疗后患血压明显下降（P＜0．01）,左室末期室间隔厚度、舒张期左室后壁厚度、左室心肌重量指数均显下降（P＜0．05）。结论：氯沙坦不但能平稳降压,而且能有效地逆转老年高血压左室肥厚。     

曲美他嗪对老年高血压伴左室肥厚患者舒张功能的改善作用

目的:观察曲美他嗪对老年高血压伴左室肥厚患者左室舒张功能的改善作用。方法:选择老年高血压伴左室肥厚患者132例,随机分为2组:治疗组,给予口服曲美他嗪20mg,每日3次;对照组给予安慰剂,每日3次;2组疗程均为1个月。以彩色多普勒超声心动图观察2组治疗前后心脏结构和舒张功能的改变情况。结果:2组治疗前后室间隔舒张末期厚度、左室后壁舒张末期厚度均无明显改变。治疗组E峰与A峰比值较治疗前明显升高(P<0.05)。结论:曲美他嗪能在不逆转高血压患者左室肥厚的情况下,明显改善左室舒张功能。     

氯沙坦对老年原发性高血压病人左心室肥厚和舒张功能的影响

目的探讨氯沙坦对老年原发性高血压病人左心室肥厚和舒张功能的影响。方法选择老年原发性高血压病人30例,给予氯沙坦治疗6个月。用M型超声心动图检测病人治疗前后舒张末期左心室内径、室间隔和左室后壁厚度,计算左心室质量指数;用多普勒超声心动图检测二尖瓣口舒张早期峰值速度（E）、舒张晚期峰值速度（A）和E峰减速时间,并计算E/A比值。结果与治疗前相比,治疗后左心室质量指数明显减少（P〈0.001）,E/A比值明显增高（P〈0.001）,E峰减速时间明显缩短（P〈0.001）。结论氯沙坦能逆转老年原发性高血压病人左心室肥厚,并改善其舒张功能。     

老年高血压病人左室肥厚与左室舒张功能的关系

目的：研究老年高血压病人左室肥厚与左室舒张功能各参数的关系,探讨在老年人左室肥厚对左室舒张功能的影响。方法：用彩色多普勒超声心动图测量101例老年高血压病人左心室结构及舒张功能参数。结果：101例高血压病人中,左室肥厚组（48例）的左房内径指数（LADI）、等容舒张时间（IVRT）、舒张期二尖瓣E波减速时间（EDT）显著大于左室正常组（53例,P〈0．05～〈0．01）．多元逐步回归分析发现,左室质量指数（LVMI）与左房射血分数（LAEF）、LADI、IVRT和EDT有明显的相关关系（r分别为0．213,0．251．0．450．0．338．P〈0．05～0．001）结论：老年高血压病人的左室增厚可进一步降低左室舒张功能。     

超声评价氯沙坦单用或与美托洛尔联用对逆转原发性高血压左室肥厚心肌的影响

目的:应用多普勒超声心动图技术观察氯沙坦、美托洛尔联合应用与单用氯沙坦在逆转原发性高血压(EH)患者左室肥厚(LVH)及改善左室舒张功能方面的疗效。方法:对EH伴LVH患者68例采用随机、单盲、彩色多普勒超声心动图测量左室重量指数(LVMI)、左室舒张功能等指标。结果:经过≥6个月治疗后,氯沙坦组(A组)、氯沙坦加美托洛尔组(B组)的血压、LVMI及左室舒张功能指标均明显改善(P<0.01),两组间结果比较:B组左室舒张功能指标较A组有统计学意义(P<0.01)。结论:氯沙坦加美托洛尔联合应用,对EH患者降压、逆转LVH的作用并不优于单用氯沙坦,但改善左室舒张功能却明显优于后者,且不良反应轻,值得临床推广应用。     

老年收缩期高血压左室肥厚与心肌缺血,室性心律失常和心 …

目的：探讨老年收缩期高血压左室肥厚与心肌缺血、心律失常、心衰间的相关性。方法：以动态心电图和超声心动图分别检测６８例老年收缩期高血压左室肥厚（ＨＬＶＨ）患者及３０例老年单纯收缩期高血压（ＳＨＴ）患者的心肌供血、心律和心功能。结果：ＨＬＶＨ组心肌缺血、室性早搏的发生率显著高于ＳＨＴ组;左室收缩功能障碍组ＬＶＥＦ,ＣＩ明显减低;左室舒张功能障碍组二尖瓣舒张早期流速（Ｅ峰）、Ｅ／Ａ、舒张早期减速度显著减     

老年高血压伴左室肥厚对左心功能的影响

目的 :探讨老年高血压伴左室肥厚对心功能的影响。方法 :应用核素心血池扫描的方法 ,对老年高血压伴左室肥厚和无左室肥厚的患者 ,进行了左室射血分数 (LVEF)、左室高峰射血率 (PER)、左室高峰充盈率(PFR)、1/ 3充盈分数 (1/ 3FF)及相角程 (PA)的测定 ,并进行比较。结果 :伴左室肥厚的患者PFR、1/ 3FF明显低于无左室肥厚的患者 ,PA明显高于无左室肥厚的患者。结论 :老年高血压伴左室肥厚对心功能的影响 ,主要表现为对舒张功能的影响 ;左室肥厚导致的心室肌纤维化、顺应性下降和运动协调性异常 ,是影响舒张功能的重要原因     

卡托普利治疗高血压左室肥厚和左室舒张功能的临床分析

目的探讨卡托普利对高血压左室肥厚与左室舒张功能的治疗作用。方法对符合ＷＨＯ诊断标准的原发性高血压病左室肥厚患者５２例,服用卡托普利治疗,用多普勒彩色超声心动图测定治疗前后左室肥厚指标,左室舒张及收缩指标。结果治疗后室间隔厚度,左室后壁厚度,左室心肌重量,左室心肌重量／左室容量均明显减小,舒张早期流速峰值明显增大,房缩期最大流速下降,两者比值下降,左室射血分数无变化。结论卡托普利可有效地抑制并逆转左室肥厚,改善左室舒张功能     

氯沙坦对高血压左心室肥厚的逆转作用

目的 :评价氯沙坦对高血压左心室肥厚的逆转作用。方法 :对 5 2例高血压左心室肥厚的患者用氯沙坦 5 0～ 10 0 mg治疗 8～ 10周后进行观察。结果 :氯沙坦治疗后血压平均下降 2 9/12 mm Hg± 5 /3mm Hg,治疗后室间隔厚度 (IVST)、心室后壁厚度 (PWT)、左室重量指数 (L VMI)均有明显减少 (均为 P<0 .0 1) ,说明左室肥厚减轻 ,左室舒张功能得到改善。结论 :氯沙坦能有确切降压效果 ,并有逆转左室肥厚的作用     

Modification of cardiac subcellular remodeling due to pressure overload by captopril and losartan

In view of the activation of renin-angiotensin system under conditions associated with pressure overload on the heart, we examined the effects of captopril, an angiotensin converting enzyme inhibitor, and losartan, an angiotensin II receptor antagonist, on cardiac function, myofibrillar ATPase and sarcoplasmic reticular (SR) Ca2+-pump (SERCA2) activities, as well as myosin and SERCA2 gene expression in hypertrophied hearts. Cardiac hypertrophy was induced in rats treated with or without captopril or losartan by banding the abdominal aorta for 8 weeks; sham operated animals served as control. Decrease in left ventricular developed pressure, +dP/dt and -dP/dt as well as increase in left ventricular end diastolic pressure and increased muscle mass due to pressure overload were prevented by captopril or losartan. Treatment of animals with captopril or losartan also attenuated the pressure overload-induced depression in myofibrillar Ca2+-stimulated ATPase, myosin ATPase, SR Ca2+-uptake and SR Ca2+-release activities. An increase in beta-myosin heavy chain mRNA and a decrease in alpha-myosin heavy chain mRNA as well as depressed SERCA2 protein and SERCA2 mRNA levels were prevented by captopril or losartan. These results suggest that both captopril and losartan improve myocardial function in cardiac hypertrophy by preventing changes in gene expression and subsequent subcellular remodeling due to pressure overload.     

氯沙坦联用葛根素对原发性高血压左心室肥厚的逆转及胰岛素抵抗的影响

目的观察氯沙坦单用或联用葛根素对原发性高血压并左室肥厚(LVH)的逆转作用及其对胰岛素抵抗的影响.方法 60例原发性高血压并左室肥厚病人随机分成两组:对照组(A组)30例口服氯沙坦,每日50 mg;治疗组(B组)30例给予氯沙坦,每日50 mg,加葛根素注射液500 mg.两组均持续治疗4周.观察左室形态结构和左室功能变化及其对胰岛素抵抗的影响.结果两组治疗后,血压水平降低,室间隔厚度(IVST)、左室后壁厚度(LVPWT)、左室舒张末期内径(LVDd)、左室重量(LVMI)均显著下降(P<0.05或P<0.01),特别是B组在逆转LVH方面效果优佳(P<0.05).与A组比较,B组治疗后2 h血糖和空腹胰岛素明显降低,而胰岛素敏感性指数明显升高.结论氯沙坦联用葛根素治疗原发性高血压,既可有效降压,又可逆转LVH以及改善胰岛素抵抗.     

一平苏对维持性血透患者心血管保护作用的临床观察

观察一平苏对维持血透患者的心血管保护作用。方法30例有高血压和左室肥厚并维持血透的患者随机分为两组,A组20例用一平苏2.5mg～5mg/d,B组给予不会影响左室重构的其它药作为对照。6个月后心脏多普勒超声检查左室重构及功能的情况。结果两组虽均有明显降压,但一平苏组治疗后LVDd,IVS,LVPWD和LVMI均有统计学意义的下降,EF和E/A均明显升高。结论一平苏不仅可安全有效地降压,还可逆转血透患者的左室肥厚及使左室舒张功能改善。     

血管紧张素Ⅱ受体拮抗剂对原发性高血压患者左心室肥厚和舒张功能的影响

目的　应用超声心动图评价血管紧张素 1型受体 ( AT1 )拮抗剂对原发性高血压患者左心室肥厚和舒张功能的影响。方法　分别于 AT1 拮抗剂 (氯沙坦 )治疗前和治疗 6个月后 ,对 3 0例原发性高血压患者进行超声心动图检查。 M型超声心动图测量舒张末期左心室内径、室间隔和左心室后壁厚度 ,计算左心室重量指数 ;在心尖左心长轴切面上 ,用多普勒超声心动图测量二尖瓣口舒张早期峰值速度 E、舒张晚期峰值速度 A和 E峰减速时间 ,并计算E/A比值。结果　氯沙坦治疗 6个月后 ,左心室重量指数从 12 4± 2 1g/m2减低为 10 2± 2 2 g/m2 ( P<0 .0 0 1) ;E/A比值 ( 1.2 5± 0 .2 7)明显高于服用前 ( 0 .94± 0 .2 6,P<0 .0 0 1) ,E峰减速时间从 2 2 1± 3 2 ms下降到 180± 2 7ms( P<0 .0 0 1)。结论　 AT1 拮抗剂氯沙坦治疗 6个月使原发性高血压患者左心室肥厚得到消退 ,并改善了其舒张功能     

Comparative effects of chronic ACE inhibition and AT1 receptor blocked losartan on cardiac hypertrophy and renal function in hypertensive patients

The present study describes the effects of losartan and the angiotensin-converting enzyme inhibitor enalapril on blood pressure, echocardiographically calculated left ventricular mass, renal function evaluated by glomerular filtration rate and quality of life. The renin-angiotensin-aldosterone system is of importance for cardiovascular growth. There is substantial experimental documentation in animals that the angiotensin II antagonist, losartan, decreases the cardiac hypertrophy response caused by elevated arterial pressure as well as intravascular volume overload. However, data in humans is scarce. This is a 3-year, randomised, double-blind study with parallel group design in 50 patients with essential hypertension. The results show that both drugs reduced blood pressure equally effectively, and also left ventricular mass (P < 0.001). After 3 years of treatment glomerular filtration rate significantly increased with losartan (P < 0.005). Serum uric acid fell modestly although significantly, dose-dependent in losartan patients compared with an increase in enalapril patients. A fall in serum potassium from the pre-study period was observed in all patients. There was no difference between treatments in terms of patient satisfaction on quality of life. Both drugs have relatively similar hormonal and haemodynamic effect, with an excellent tolerability profile; they appear to induce comparable blood pressure falls in hypertensive patients in particular, therapy based on specific Ang II blockade may offer advantages in high risk hypertensives if left ventricular hypertrophy is present. Both enalapril and losartan, in improving the renal function attenuating the intrarenal effects of angiotensin II, might be able to reverse the pathophysiology of essential hypertensive kidney disease, and should be first-choice drugs in the treatment of essential hypertension.     

氯沙坦对老年高血压病患者心室肥大和QTd的影响

目的　评价氯沙坦对老年原发性高血压病患者左心室肥大及 QT离散度 (QTd)的影响。方法　依据是否伴有左心室肥大 ,将 5 7例轻、中度高血压病患者分为两组 ,分别给予氯沙坦 5 0 mg/d,或氯沙坦 5 0 m g/d加双氢克尿噻12 .5 mg/d治疗 ,共 16～ 18周 ,比较两组治疗前后左心室大小 ,及 QTd改变 ,并分析 L VMI与 QTd的相关性。结果　治疗后高血压伴左心室肥大组 L VDd,IVST,PWT,L VMI比治疗前下降 (P<0 .0 5或 P<0 .0 1)。高血压伴左心室肥大组 QTd比不伴左心室肥大组大 (P<0 .0 1) ,治疗后则明显减小 (P<0 .0 1)。高血压伴左心室肥大组 L VMI与 QTd有较好的相关性。结论　氯沙坦或氯沙坦加双氢克尿噻能逆转老年高血压病患者的左心室肥大 ,并使 QTd相应减小。     

Transforming growth factor beta in hypertensives with cardiorenal damage

We investigated whether a relationship exists between circulating transforming growth factor beta -1 (TGF-beta(1)), collagen type I metabolism, microalbuminuria, and left ventricular hypertrophy in essential hypertension and whether the ability of the angiotensin II type 1 receptor antagonist losartan to correct microalbuminuria and regress left ventricular hypertrophy in hypertensives is related to changes in TGF-beta(1) and collagen type I metabolism. The study was performed in 30 normotensive healthy controls and 30 patients with never-treated essential hypertension classified into 2 groups: those with microalbuminuria (urinary albumin excretion >30 and <300 mg/24 h) associated with left ventricular hypertrophy (left ventricular mass index >116 g/m(2) for men and >104 g/m(2) for women) (group B; n=17) and those without microalbuminuria or left ventricular hypertrophy (group A; n=13). The measurements were repeated in all patients after 6 months of treatment with losartan (50 mg once daily). The serum concentration of TGF-beta(1) was measured by a 2-site ELISA method, and the serum concentrations of carboxy-terminal propeptide of procollagen type I (a marker of collagen type I synthesis) and carboxy-terminal telopeptide of collagen type I (a marker of collagen type I degradation) were measured by specific radioimmunoassays. The duration of hypertension and baseline values of blood pressure were similar in the 2 groups of patients. No differences in serum TGF-beta(1), carboxy-terminal propeptide of procollagen type I, and carboxy-terminal telopeptide of collagen type I were found between normotensives and group A of hypertensives. Serum TGF-beta(1), carboxy-terminal propeptide of procollagen type I, and the ratio of carboxy-terminal propeptide of procollagen type I to carboxy-terminal telopeptide of collagen type I were increased (P<0.05) in group B of hypertensives compared with group A of hypertensives and normotensives. No differences in carboxy-terminal telopeptide of collagen type I were found among the 3 groups of subjects. After treatment with losartan, microalbuminuria and left ventricular hypertrophy persisted in 6 patients (then considered nonresponders) and disappeared in 11 patients (then considered responders) from group B. Compared with nonresponders, responders exhibited similar control of blood pressure and higher (P<0.05) blockade of angiotensin II type 1 receptors (as assessed by a higher increase in plasma levels of angiotensin II). Whereas TGF-beta(1), carboxy-terminal propeptide of procollagen type I, and the ratio of carboxy-terminal propeptide of procollagen type I to carboxy-terminal telopeptide of collagen type I decreased (P<0.05) in responders, no changes in these parameters were observed in nonresponders. These findings show that an association exists between an excess of TGF-beta(1), stimulation of collagen type I synthesis, inhibition of collagen type I degradation, and cardiorenal damage in a group of patients with essential hypertension. In addition, our results suggest that the ability of losartan to blunt the synthesis of TGF-beta(1) and normalize collagen type I metabolism may contribute to protect the heart and the kidney in a fraction of patients with essential hypertension.