氯沙坦治疗高血压病及逆转左室肥厚的临床观察

目的:探讨氯沙坦治疗高血压病的疗效和对左室肥厚(LVH)的逆转作用。方法:选择78例伴有左室肥厚的高血压病患者,随机分为氯沙坦治疗组(A组,48例),和复方降压片治疗组(B组,30例),A组服用氯沙坦50-100 mg/d,B组用复方降压片治疗,疗程均为10-12周,治疗前后两组分别进行偶测血压及超声心动图等检测。结果:A、B两组均能显著降低血压,两组对偶测血压下降幅度无显著性差异(P>0.05),治疗12周后A组室间隔与左室后壁厚度较治疗前显著改善(P>0.01),B组无明显改变。结论:氯沙坦能有效控制高血压患者的血压并有效逆转左室肥厚。     

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。     

赖诺普利与非洛地平缓释片联用对高血压伴左室肥厚的逆转作用

目的 :观察赖诺普利与非洛地平联用对原发性高血压 (EH)伴左室肥厚 (LVH)的逆转效果。方法 :将 82例EH伴LVH患者随机分为A组 (单用赖诺普利 ) 4 0例 ,B组 (赖诺普利与非洛地平缓释片联用 ) 4 2例。观察两组治疗前后及两组间血压及LVH指标的变化。结果 :6个月后两组血压均较治疗前明显下降 (P <0 .0 1) ,组间降压幅度差异无显著性意义 (P >0 .0 5 ) ;两组左室重量指数均较治疗前明显降低 (P <0 .0 1) ,B组较A组更明显 (P <0 .0 5 )。结论 :两药联用对LVH逆转有协同作用。     

替米沙坦对原发性高血压左室肥厚的影响

目的评价血管紧张素Ⅱ（AngⅡ）受体拮抗剂替米沙坦降压疗效及对原发性高血压（EH）左室肥厚（LVH）的逆转作用.方法对64例EH伴LVH者给予口服替米沙坦片每日40 mg～80 mg,每日1次,疗程20周,每周测血压1次,并用超声心动图观察治疗前后LVH和左室舒张功能的改变.结果与治疗前比较,64例EH病人的收缩压和舒张压均明显降低（P〈0.01）,舒张期室间隔厚度、左室后壁厚度、左室重量指数明显减少（P〈0.01）.结论替米沙坦能有效地控制血压,且对高血压左室肥厚有逆转作用.     

氯沙坦钾对原发性高血压患者左室肥厚逆转作用

目的　研究氯沙坦钾对原发性高血压 (EH)患者的降压作用和对左室肥厚 (LVH)的影响。　方法　选择 4 8例EH患者 ,其中有LVH者 2 4例 ,口服氯沙坦钾 5 0mg d ,为期半年。　结果　治疗后血压明显下降 (P <0 0 1) ,并且二维超声心电图参数也显示有左室肥厚逆转变化 (P <0 0 5 ,P <0 0 1)。　结论　EH患者经氯沙坦钾治疗后 ,能有效控制血压 (P <0 0 1) ,并能逆转左室肥厚。     

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52例高血压左心室肥厚的患者用氯沙坦50～100 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29/12 mmHg±5/3 mmHg , 治疗后室间隔厚度 (IVST) 、心室后壁厚度(PWT)、左室重量指数(LVMI)均有明显减少(均为P<0.01),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.     

替米沙坦逆转原发性高血压心肌肥厚的作用

目的 :观察替米沙坦降压疗效及对原发性高血压 (EH)左室肥厚 (LVH)的逆转作用。方法 :对 33例EH并LVH者给予口服替米沙坦片 4 0～ 80mg ,每日 1次 ,疗程 12周 ,每周测血压 1次 ,并用超声心动图观察治疗前后LVH和左室舒张功能的改变。结果 :替米沙坦可有效降低EH患者的收缩压和舒张压 ,明显改善舒张期室间隔厚度、左室后壁厚度 ,且左室重量指数较治疗前明显减少 (P <0 .0 1)。结论 :替米沙坦能有效地控制血压 ,且对EH的LVH有逆转作用。     

安博维抗高血压及逆转左室肥厚和舒张功能异常的作用

目的:观察安博维降压疗效及对原发性高血压(EH)左室肥厚(LVH)及舒张功能异常(ADF)的逆转作用.方法:42例患者口服安博维150mg,晨顿服1次,治疗12周.用超声心动图测定患者的左室肥厚和舒张功能异常的改善情况.结果:安博维使24h血压稳定下降,左室质量指数减低(P<0.01).结论:安博维能有效治疗高血压,有逆转左室肥厚及舒张功能异常的作用.     

氯沙坦联合依那普利对高血压心肌肥厚患者左室舒张功能的影响

目的 观察氯沙坦联合依那普利对高血压心肌肥厚患者左心室舒张功能的影响.方法 采用自身对照设计,36例坚持随访均患者给予氯沙坦50mg/次,每天一次;依那普利10mg/次～20mg/次,每天一次,随访24周,期间比较血压的变化;治疗前后作超声心动图检查,比较心肌厚度及左室舒张功能的改变.结果 与治疗前相比,患者左室后壁舒张末期厚度(LVPWT)、室间隔舒张末期厚度(IVST)、均明显下降(P<0.01);反映左室舒张功能的A/E值亦较治疗前下降(P<0.05);收缩压与舒张压均明显降低(P<0.01). 结论 氯沙坦与依那普利联合用药能有效地控制血压、逆转左室肥厚、改善左心室舒张功能.     

左旋氨氯地平联合培哚普利治疗老年高血压合并左室肥厚的疗效

目的 探讨左旋氨氯地平联合培哚普利治疗老年原发性高血压(EH)合并左室肥厚(LVH)患者的临床效果.方法 将80例EH伴LVH患者随机分为两组(年龄均≥60岁),对照组40例,治疗组40例.两组均给予苯磺酸左旋氨氯地平(施慧达,吉林天风制药公司)2.5～5 mg,1次/d;治疗组联合培哚普利(雅施达,天津施维雅制药公司)4～8 mg,1次/d,晨起顿服.治疗24 w,观察降压疗效和LVH改善情况.结果 两组均能有效降低血压,逆转左室肥厚.治疗组降压总有效率95%,对照组82.5%,治疗组血压下降显著,两组间差异有显著性(P＜0.05);治疗组左室舒张末期室间隔厚度(IVST)、左室后壁舒张末期厚度(LVPWT)及左室心肌重量指数(LVMI)均较对照组改善显著,差异均有显著性(P＜0.05).结论 两药联合服用对老年EH伴LVH有协同逆转作用,可作为治疗EH伴LVH患者尤其是老年人的一线用药.     

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。     

细胞内游离钙、血压变异性在氯沙坦逆转高血压左心室肥厚中的作用

目的　探讨原发性高血压 ( EH)患者淋巴细胞内胞浆游离钙浓度 ( [Ca2 + ] i)、血压变异性 ( BPV)与氯沙坦逆转高血压左心室肥厚作用的关系。方法　选择 EH患者 60例 ,予氯沙坦治疗 6个月 ,治疗前后检测 [Ca2 + ] i、BPV及左心室重量指数 ( LVMI)。结果　经氯沙坦治疗后 ,EH患者淋巴细胞内 [Ca2 + ] i 从治疗前的 10 2 .3± 11.84nmol/ L降至 84.64± 9.5 2 nmol/ L( P<0 .0 1) ,LVMI从治疗前的 15 5 .69± 2 1.75 g/ m2降至 13 5 .85± 13 .66g/ m2 ( P<0 .0 0 1) ,BPV亦显著下降 ( P<0 .0 1)。 [Ca2 + ] i 的下降幅度与 LVMI的下降幅度呈显著正相关 ( r=0 .6675 ,P<0 .0 5 )。结论　氯沙坦能降低高血压病患者的 BPV,逆转高血压左心室肥厚 ,其逆转左心室肥厚的作用可能与降低血管紧张素 引起的 [Ca2 + ] i 升高有关     

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     

氯沙坦对高血压左室肥厚患者血浆脑钠肽的影响

目的：研究氯沙坦干预对高血压伴左室肥厚患者脑钠肽（BNP）的影响及意义。方法：选择100例左室射血分数正常范围的高血压患者,其中58例伴左室肥厚,42例不伴左室肥厚,另选50例健康者作为健康对照组,比较三组间血浆BNP水平。左室肥厚组给予氯沙坦治疗6个月,比较治疗前后BNP、左室质量指数（LVMI）的变化。结果：①高血压伴左室肥厚患者BNP浓度显著高于不伴左室肥厚组及健康对照组[（62．21±9．70）pg／ml比（39．35±10．57）pg／ml比（13．89±5．34）pg／ml,P〈0．01];②BNP的浓度与LVMI呈正相关（r=0．44,P〈0．05）;③与治疗前比较,氯沙坦治疗高血压伴左室肥厚6个月后,血浆BNP[（62．21±9．70）pg／ml比（38．78±7．94）pg／m1]、LVMI[（128．71±12．64）g／m。比（107．36±11．32）g／m。]均显著降低（P〈o．01）。结论：氯沙坦可明显降低高血压伴左室肥厚患者脑钠肽水平,逆转左室肥厚。     

高血压病患者左室肥厚及构型改变与胰岛素抵抗的关系

目的:探讨高血压病(EH)患者胰岛素抵抗(IR)对左心室肥厚(LVH)和几何构型的影响。方法:检测124 例EH病人的左室重量指数(LVMI),相对室壁厚度(RWT),空腹血清葡萄糖(FSG)、空腹血胰岛素(FSI)浓度, 并计算胰岛素敏感性指数(ISI)。依照LVMI及RWT的数值124例EH病人被分为左室正常构型(51例),向心性构型(30例),向心性肥厚型(22例),离心性肥厚型(21例)。结果:RWT与年龄、体重指数(BMI)、收缩压(SBP)、舒张压(DBP)、平均心率呈正相关(r=0.16-0.22,P<0.05),与ISI呈负相关(r=-0.24),LVMI与SBP、DBP呈正相关(r=0.16-0.20,P<0.05),与ISI不相关。向心性重构组和向心性肥厚组年龄、RWT、HR、BMI大于正常构型组(P<0.05-<0.01),而ISI小于正常构型组(P<0.01)。结论:胰岛素敏感性降低与EH患者左心室肥厚无关,与RWT增加密切相关;ISI可能是EH患者发生左室向心性构型的重要影响因素之一。     

胰岛素抵抗与原发性高血压左室肥厚关系的研究

目的　探讨胰岛素抵抗 (IR)对原发性高血压 (EH)患者左室肥厚的影响。方法　检测 93例 EH病人的左室心肌重量指数 (LVMI)、相对室壁厚度 (RWT)、空腹血糖 (FSG)、空腹血胰岛素 (FSI) ,并计算胰岛素抵抗指数 (IRI)。设对照组 48例。结果　 IRI在对照组与 EH各组比较差异呈显著性 (P<0 .0 1 ) ,但在 EH各组间差异无显著性 (P>0 .0 5)。 IRI在 EH各组间与 RWT呈正相关 (P<0 .0 1 ) ,与 LVMI不相关 (P>0 .0 5)。结论　 IR存在于 EH患者中 ,与 RWT的增加有密切的关系 ,高胰岛素血症是 EH患者发生左室肥厚的重要因素。     

科素亚对原发性高血压左心室肥厚及血浆纤维蛋白原的影响

目的　观察科素亚对原发性高血压患者左心室肥厚 (L VH)及血浆纤维蛋白原的影响。方法　选择 5 4例原发性高血压伴左心室肥厚病人 ,随机分成两组分别予科素亚 5 0～ 10 0 mg/d或科素亚 2 5～ 5 0 m g/d加用卡托普利 37.5～ 75 m g/d降压治疗半年 ,治疗前后分别测定左心室质量指数 (L VMI)及血浆纤维蛋白原 (Fg)水平。结果　与治疗前比较 ,无论科素亚或科素亚加卡托普利均使 L VMI及 Fg降低 ,科素亚加卡托普利降低的程度更大。结论　科素亚与卡托普利联合应用后逆转左心室肥厚的效果更好 ,同时可降低 Fg     

Effects of losartan and atenolol on left ventricular mass and neurohormonal profile in patients with essential hypertension and left ventricular hypertrophy

OBJECTIVE: To compare the effects of the angiotensin II antagonist, losartan, with those of atenolol on left ventricular hypertrophy (LVH), blood pressure and neurohormone concentrations in hypertensive patients with LVH. DESIGN: A multinational, randomized, double-blind trial. SETTING: Hospital. PATIENTS: Hypertensive patients with an echocardiographically documented left ventricular mass index (LVMI) 120 g/m(2) (men) or 105 g/m(2) (women). INTERVENTIONS: Patients allocated randomly to groups received either losartan or atenolol 50 mg/day for 36 weeks, with possible titration to 100 mg/day, and addition of hydrochlorothiazide 12.5 or 25 mg/day. MAIN OUTCOME MEASURES: Changes in LVMI and sitting systolic (SBP) and diastolic (DBP) blood pressures after 36 weeks of treatment (study powered for non-inferiority hypothesis). All echocardiographic data were read in a central laboratory by staff blinded to the treatments and sequence of echocardiographic tapes. RESULTS: The estimated treatment difference between the losartan and atenolol regimens (mean change from baseline at week 36) in LVMI was -2.5 g/m(2) [95% confidence interval (CI) -7.36 to 2.37 g/m(2) ] in favor of losartan, indicating that losartan was significantly non-inferior ( 0.001, non-inferiority limit 8 g/m(2) ) and numerically superior to atenolol in reducing LVMI. The losartan-based regimen significantly reduced LVMI after 36 weeks compared with baseline (-6.56 g/m(2) , 95% CI -10.24 to -2.88 g/m(2) , P<0.001), whereas the atenolol-based regimen had no significant effect (-3.71 g/m, 95% CI -7.75 to 0.32 g/m(2) , P= NS). In a subset of 82 patients, significant changes in serum concentrations of atrial natriuretic peptide, brain natriuretic peptide and immunoreactive amino-terminal pro-brain natriuretic peptide were recorded in losartan-treated ( 0.01) but not atenolol-treated patients. Losartan and atenolol significantly decreased SBP and DBP from baseline after 6, 12, 24 and 36 weeks. The changes from baseline in DBP were greater in the atenolol group at weeks 6 and 36 [difference -2.6 mmHg ( P= 0.016) at week 36]. However, both treatment regimens achieved similar SBP/DBP values at week 36 (141.1 +/- 12.8/86.8 +/- 8.2 mmHg for losartan and 141.4 +/- 17.2/85.0 +/- 10.1 mmHg for atenolol, respectively). Overall, losartan treatment was associated with significantly fewer drug-related clinical adverse events, compared with atenolol (10 and 22%, respectively, P= 0.028). CONCLUSIONS: Both losartan- and atenolol-based regimens effectively decreased blood pressure. Losartan was non-inferior and numerically superior to atenolol in regression of LVH. The reduction in hypertrophy with losartan treatment was accompanied by reductions in circulating concentrations of cardiac natriuretic peptides. Losartan, by specifically blocking angiotensin II, may therefore have effects on the heart beyond those expected from the decrease in blood pressure alone. Losartan was better tolerated than atenolol.     

葛根素对高血压病患者左室肥厚的影响

目的 探讨葛根素对高血压病患者左室肥厚的影响及可能的机制。 方法58例原发性高血压伴左室肥厚患者,随机分为对照组(28例)及葛根素组(30例),对照组予罗布麻、双氢克尿噻降压治疗,葛根素组在此基础上合用葛根素片195mg/d,疗程均为6个月,观察左室质量指数(LVMI)及血浆自由脂肪酸(FFA)、内皮素-1(ET-1)、一氧化氮(NO)的变化。 结果葛根素组LVMI、FFA、ET-1降低,NO增加(P<0.01),其LVMI的变化与FFA、ET-1的改变呈正相关(r=0.41,0.44,P<0.05),而与NO的改变呈负相关(r=-0.37,P<0.05),对照组无明显变化(P>0.05)。 结论葛根素逆转高血压病患者左室肥厚,可能与改善内皮功能及脂肪酸代谢有关。     

Relation of insulin resistance and left ventricular function and structure in non-diabetic patients with essential hypertension

OBJECTIVE: Both left ventricular hypertrophy and insulin resistance (IR) have often been demonstrated in patients with essential hypertension (EH). Insulin may exert a direct growth-promoting effect on cardiomyocytes. The purpose of this study was to examine the relationship between left ventricular structure, function and IR in patients with EH. METHODS: We enrolled 73 patients (21 men, mean age 51.7 +/- 9.2 years) with untreated hypertension (BP > 140 and/or 90 mm Hg, fasting glycaemia < 110 mg/dl) and 64 healthy subjects without diabetes mellitus and hypertension (21 men, mean age 48.9 +/- 10.6 years) constituted the control group. In all subjects, transthoracic echocardiography was performed and blood samples were taken. Homeostasis model assessment (HOMA) was calculated by the formula: HOMA-index = fasting blood glucose (mg/dl) * immunoreactive insulin (microU/ml)/405 for the assessment of IR. Hypertensive patients were divided in two groups by mean HOMA index values. Each subject was examined for LV end-diastolic diameter, septal and posterior wall thickness, LV mass index (LVMI), fractional shortening (FS), mitral inflow velocity pattern, atrial filling fraction (AFF), left ventricular outflow velocity pattern and the total ejection isovolume index (TEI index). RESULTS: The HOMA index (p < 0.001), LVMI (p < 0.001), AFF (p < 0.0001), peak A velocity (p < 0.028), septal (p < 0.0001) and posterior (p < 0.0001) wall thickness were significantly higher and FS (p < 0.001), E/A ratio (p < 0.0001) were significantly lower in hypertensive patients than healthy controls. LVMI (p < 0.01) and septal wall thickness (p < 0.001) were significantly higher in those hypertensive patients with a higher HOMA index. The HOMA-index was univariately related to the TEI index (r = 0.27, p = 0.01) and septal wall thickness (IVS) (r = 0.29, p = 0.01) by Pearson correlation analysis in hypertensive patients. LVMI, FS and mitral inflow velocity pattern were not related to the HOMA index. The TEI index (R2 = 0.20, p = 0.0001) and IVS (R2 = 0.12, p = 0.002) were significantly related to the HOMA-index as an independent variable by stepwise regression analysis. CONCLUSIONS: These results demonstrated that hypertensive patients had both abnormal cardiac structure and function and higher IR index. In our study group, the effect of hypertension on cardiac structure and function was correlated with IR. Our results suggested that IR might be an important factor causing left ventricular dysfunction and wall thickness in non-diabetic patients with EH.