赖诺普利逆转高血压患者左室肥厚的相关性研究

目的探讨赖诺普利对高血压患者左室肥厚的逆转作用。方法分别口服赖诺普利与卡托普利治疗高血压伴左室肥厚患者8周,应用超声心动图监测治疗前、后左室重量指数（LVMI）,同时采用放射免疫法和（或）化学发光法检测血浆血管紧张素Ⅱ（AT-Ⅱ）醛固酮（ALD）,血清胰岛素样生长因子-1（IGF-1）的浓度。结果①高血压组患者血浆AT-Ⅱ、ALD,血清IGF-1浓度明显高于正常对照组（P值分别为0.023,0.018,0.032）,LVH组高于无LVH组（P值为0.0083）。②治疗后与治疗前比较,两组患者AT-Ⅱ、ALD、IGF-1和LVMI水平均显著降低（P值分别为0.036,0.028,0.031）,但赖诺普利组降低幅度明显高于卡托普利组,差异有统计学意义（P〈0.01）。结论赖诺普利与卡托普利均有降压及逆转左室肥厚的作用,但赖诺普利逆转LVH的强度更强,且不良反应少,依从性强,值得临床推广使用。     

非洛地平与赖诺普利的降压效应及对左室肥厚逆转作用的对比

目的：评价并比较非洛地平及赖诺普利治疗轻、中度原发性高血压（ＥＨ）的降压疗效及对左心室肥厚的逆转作用。方法：选择１２８例轻、中度ＥＨ患者,入选前服用安慰剂２周,随机分为非洛地平组６６例和赖诺普利组６２例。非洛地平组服用非洛地平５～１０ｍｇ／ｄ,赖诺普利组服用赖诺普利１０～２０ｍｇ／ｄ,每日１次,疗程２４周。两组均在治疗前及治疗后的２、１２、２４周分别进行偶测血压、２４ｈ动态血压及超声心动图检查。结果：非洛地平和赖诺普利均能显著降低血压,两药对偶测血压的下降幅度差异无显著性（Ｐ＞０．０５）。非洛地平能有效控制清晨高峰期血压。收缩压、舒张压的谷／峰比值分别是７２％、６７％。非洛地平降低２４ｈ平均血压和白昼血压的幅度大于赖诺普利,而夜间血压降低的幅度显著低于白昼。两药治疗２４周后,室间隔厚度、左心室后壁厚度、左室心肌重量及左室重量指数较治疗前显著改善（Ｐ＜０．００１）。两组药物副反应均较轻。结论：非洛地平能有效降低ＥＨ患者的血压,降低靶器官损害的危险性。     

赖诺普利治疗高血压病的临床疗效观察

赖诺普利治疗高血压病的临床疗效观察（摘要）张敏州陈锡龙陈次滨沈彦张育君曾群英丁有钦黄洋浩用随机单盲法将１０８例轻、中度高血压病患者分成２组，用卡托普利（ｃａｐｔｏｐｒｉｌ）作对照，观察赖诺普利（ｌｉｓｉｎｏｐｒｉｌ）的降压效果和不良反应，疗程６周。...     

赖诺普利与依那普利治疗高血压病的对比研究

本研究用随机、单盲、组间、平行对照的方法，用新一代血管紧张素转换酶抑制剂赖诺普利对高血压病患者进行为期４周的治疗观察，并与另一种血管紧张素转换酶抑制剂依那普利进行对比。赖诺普利剂量为１０～８０ｍｇ／ｄ；依那普利为５～４０ｍｇ／ｄ，每天１次服用。通过２２５例的观察显示两药的降压有效率无明显差异，但赖诺普利控制２４小时的血压明显较依那普利为优，不良反应的发生率赖诺普利较依那普利为少。咳嗽的发生率两药相仿。赖诺普利有效病例的平均剂量为３４．１ｍｇ／ｄ，故建议常用剂量为１０～４０ｍｇ／ｄ，每日早餐后服用。研究证实赖诺普利是一安全、有效的降压药。     

赖诺普利在老年高血压病治疗中降压及逆转左心室肥厚的效果观察

目的探讨赖诺普利在老年高血压病治疗中降压及逆转左心室肥厚的效果。方法选取48例原发性高血压患者，给予赖诺普利每日10mg治疗，每2周随访1次，随访12周，监测血压，疗效不佳者加用赖诺普利10mg或加用氢氯噻嗪12．5mg／d，24周以后复查彩色多普勒超声心动图，取胸骨旁左室长轴切面二维超声图像，在二尖瓣水平的M型图像测定舒张末期室间隔厚度（IVST），左室舒张末期内径（LVDd），左室射血分数（LVEF）。结果治疗第2周随访时，显效率58．3％（28例），总有效率79．1％（38例）。第12周随访时，显效率70．8％（34例），总有效率89．6％（43例）。第24周时舒张末期室间隔厚度（IVST）、左室舒张末期内径（LVDd）、左室射血分数（LVEF）与治疗前对比差异有统计学意义（P〈0．01）。结论赖诺普利有明显降血压和逆转左心室肥厚的作用。     

比索洛尔、拉西地平和赖诺普利对高血压病患者24小时血压的影响

目的比较比索洛尔、拉西地平和赖诺普利对２９例高血压病患者的降压疗效。方法采用随机、单盲和交叉的方法，运用２４小时动态血压监测。结果三药均能显著降低血压，彼此间降低偶测血压的幅度无显著差异。比索洛尔和拉西地平降低２４小时平均和白天平均血压的幅度大于赖诺普利。三药均能有效控制清晨血压高峰期的血压，它们的降压谷／峰比值都超过６５％。结论比索洛尔、拉西地平和赖诺普利均可每日服用１次，前二药控制２４小时血压及清晨醒后的高峰期血压较后者为佳。     

赖诺普利治疗高血压病及逆转左室肥厚的疗效观察

目的观察赖诺普利对1级～2级高血压病病人的降压效果及对左室肥厚的逆转作用.方法选择43例1级～2级高血压病并左室肥厚病人,给予赖诺普利10 mg/d,2周后如舒张压>90 mmHg,则剂量加倍,4周后如仍无效则加用氢氯噻嗪25 mg/d,疗程12周,治疗前后测血压,并进行二维超声心动图检查.结果赖诺普利能显著降低高血压病病人的血压,有效率达93.0%,其中16.3%病人加用利尿剂,治疗前后比较有统计学意义(P<0.01),室间隔厚度、左心室后壁厚度较治疗前亦明显改善(P<0.01). 结论赖诺普利能够降低血压,逆转左室肥厚,减轻靶器官损害.     

赖诺普利与氨氯地平对老年性高血压患者左心室质量及舒张功能影响的Meta分析

目的系统评价赖诺普利与氨氯地平对老年性高血压患者左心室质量及舒张功能的影响。方法计算机检索Cochrane Library、Pubmed、EMBASE、中国学术期刊网络出版总库、中国生物医学文献数据库、维普、万方,从各数据库建库至2012年11月,纳入赖诺普利与氨氯地平治疗老年性高血压的RCT文献,按纳入与排除标准选择文献并评价质量后,用Revman 5.1软件进行Meta分析。结果共纳入4篇随机对照试验,408例患者。Meta分析结果显示:赖诺普利与氨氯地平在减小左室心肌重量指数[MD=-9.79 95%CI(-27.70,8.12),P=0.28]、左室舒张末期内径[MD=0.22 95%CI(-1.57,2.01),P=0.81]、舒张期室间隔厚度[MD=-0.94 95%CI(-3.16,1.27),P=0.40]、左心室后壁厚度[MD=-1.689 5%CI(-4.82,1.45),P=0.29]、左心室质量[MD=-6.64 95%CI(-15.84,2.56),P=0.16]、收缩压[MD=0.42 95%CI(-2.41,3.25),P=0.77]、舒张压[MD=0.80 95%CI(-1.13,2.73),P=0.42]方面的差异无统计学意义。而在增加E/A比值[MD=0.07 95%CI(0.00,0.13),P=0.04]方面,氨氯地平优于赖诺普利。结论赖诺普利与氨氯地平在减少左心室质量,提高舒张功能方面的差异并不明显。但从药品经济学观点考虑,赖诺普利具有更好的成本-效果比。     

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。     

赖诺普利与依那普利治疗轻、中度高血压病的疗效比较

目的：比较赖诺普利与依那普利治疗轻、中度高血压病的疗效和安全性。方法：随机开放对照试验，经1周药物冲洗期及2周安慰剂导入期，218例轻、中度高血压患进入8周的治疗期，每日1次服用赖诺普利10mg(118例）或依那普利5mg(100例），2周后如坐位舒张压≥90mmHg则剂量加倍，4周后如仍无效则每日加服双氢克尿噻25mg。每组各随机选择10例患于导入期末及治疗期末行24小时ABPM。结果：两组药物均能明显降低血压（P＜0．001）赖诺普利有效率94．1％，依那普利有效率96．0％，两组无显差异（P＞0．05）。赖诺普利和依那普利分别有33．3％和46．0％患加用利尿剂（P＞0．05）。降压谷峰值赖诺普利为56．4％／64．8％，依那普利为49．4％／22．6％。最常见不良反应是咳嗽，两组分别为9．3％和10．0％。结论：对于轻、中度高血压病赖诺普利是一种有效、安全且易耐受的降压药，每日1次能维持24小时降压效应。     

Postinfarction left ventricular remodeling in patients with hypertension

1-3 years after myocardial infarction 140 patients (66 with - group 1, and 74 without - group 2 - hypertension before infarction) were examined by echocardiography. In group 1 concentric remodeling was found in 71.4% of patients with postinfarction scar occupying 相似文献   

氨氯地平对高血压病病人左心室 构的影响

目的：观察氨氯地平第三代二氢吡啶类钙拮抗剂对高血压病病人左心室向心性重构的影响。方法在6个月的随机单试验中,利用M型和多普勒超声心动图观察氨氯地平（5mg/d)对60例未经治疗的原发性高血压合并左心室向心性重构患者的左心室室壁厚度、左心室重量以及左心室重量指数的影响。结果氨氯地平可明显降低患者的收缩压以及舒张压（P＜0．01）,在降低血压的,氨氯地平降低左心室室壁厚度（P＜0．01）、左心室重量（P＜0．05）和左心室重量指数（P＜0．01）。结论氨氯地平应用半年后,在平稳降压的同时可使向性左室重构及左心室肥厚逆转。     

Correlation of left ventricular hypertrophy and its regression by lisinopril with salt-induced hypertension

The interaction of salt with hypertension-induced left ventricular hypertrophy and its reversal by inhibition of angiotensin converting enzyme were studied in salt sensitive and salt resistant Dahl rats. Eight-week-old rats were fed either a low or high salt diet for three weeks. The colonies were then further divided and either treated with lisinopril or given no treatment for 11 weeks. Untreated salt sensitive rats had higher blood pressures than salt resistant animals. Left ventricular weight and wall thickness in both untreated salt sensitive groups was higher than in the resistant groups. Therapy lowered blood pressures in all groups but those of the high salt group remained higher than the low salt group. Reduction of left ventricular weight and wall thickness took place in either strain only when salt intake was low. Right ventricular and atrial weights were largely unaffected either by salt intake or drug therapy. Plasma renin activity increased and aldosterone levels decreased with lisinopril therapy in all groups except the salt sensitive, high salt group where both remained unchanged at low levels. Lisinopril was effective in reducing blood pressure and left ventricular hypertrophy, but both effects were severely impaired by high salt intake. The major determinant of left ventricular hypertrophy appeared to be afterload, as shown by a good correlation between left ventricular mass and systolic blood pressure, but there was some indication of a possible independent hypertrophic action of salt.(ABSTRACT TRUNCATED AT 250 WORDS)     

直接经皮冠状动脉介入治疗对急性前壁心肌梗死并室壁瘤患者心室重构和心功能关系的对比研究

目的　观察和评价直接经皮冠状动脉介入治疗 ( PCI)对急性前壁心肌梗死 ( AMI)合并室壁瘤形成患者左心室重构和心功能的影响。方法　对发病后 12 h以内入院的首次前壁 AMI患者行 PCI、尿激酶静脉溶栓、AMI常规治疗。所有患者均在治疗后 2周行超声心动图 ( UCG)筛查有无室壁瘤形成。入选有室壁瘤者并于 2周、12周、2 4周行 UCG检查。结果　共入选患者 76例 ,其中PCI组 2 8例 ( A组 ) ,溶栓组 2 6例 ( B组 ) ,对照组 2 2例 ( C组 )。结果显示 :( 1)治疗后 2周 ,A组左心室收缩末期容积指数( LVESVI)、左心室舒张末期容积指数 ( LVEDVI)、左心室质量指数 ( L VMI)、局部室壁运动指数 ( RWMI)低于 C组 ( P均 <0 .0 5 ) ,左心室射血分数 ( LVEF)高于 C组 [( 4 8.3 3± 4.5 6) % vs( 3 5 .3 3± 4.2 8) % ,P<0 .0 5 ] ;B组 L VESVI、LVEDVI、LVMI、RWMI低于 C组 ( P均 <0 .0 5 ) ,L VEF高于 C组 ( P<0 .0 5 ) ;A组 LVESVI、L VEDVI低于 B组 ( P均 <0 .0 5 ) ,L VEF高于 B组 ( P<0 .0 5 )。( 2 )治疗后 12周 ,A组 LVESVI、L VEDVI低于 B组 ( P均 <0 .0 5 ) ;A、B组 LVESVI、L VEDVI、L VMI、RWMI均低于 C组 ( P均<0 .0 5 ) ,L VEF均高于 C组 ( P均 <0 .0 5 )。 ( 3 )治疗后 2 4周 A组 L VESVI仍低于 B组 3 6.60     

Cardioreparative effects of lisinopril in rats with genetic hypertension and left ventricular hypertrophy.

BACKGROUND. In genetic and acquired hypertension, a structural remodeling of the nonmyocyte compartment of the myocardium, including the accumulation of fibrillar collagen within the interstitium and adventitia of intramyocardial coronary arteries and a medial thickening of these vessels, represents a determinant of pathological hypertrophy that leads to ventricular dysfunction. METHODS AND RESULTS. To evaluate the benefit of angiotensin converting enzyme inhibition in reversing this interstitial and vascular remodeling in the rat with genetic spontaneous hypertension (SHR) and established left ventricular hypertrophy (LVH), we treated 14-week-old male SHR with oral lisinopril (average dose, 15 mg/kg/day) for 12 weeks. Myocardial stiffness and coronary vascular reserve to adenosine (800 micrograms/min) were examined in the isolated heart; myocardial collagen and intramural coronary artery architecture were analyzed morphometrically. In lisinopril-treated SHR compared with 14-week-old baseline or 26-week-old untreated SHR and age- and sex-matched Wistar-Kyoto (WKY) controls, we found 1) a regression in LVH and normalization of blood pressure, 2) a complete regression of interstitial fibrosis, represented by a decrease of interstitial collagen volume fraction from 7.0 +/- 1.3% to 3.2 +/- 0.3% (p less than 0.025; WKY, 2.8 +/- 0.5%), 3) normalization of myocardial stiffness constant from 19.5 +/- 0.9 to 13.7 +/- 1.3 (p less than 0.025; WKY, 13.8 +/- 2.2), 4) a reversal of intramural coronary artery remodeling, including a decrease in the ratio of perivascular fibrosis to vessel lumen size from 1.4 +/- 0.2 to 0.4 +/- 0.1 (p less than 0.025; WKY, 0.6 +/- 0.1) and medial thickening from 12.3 +/- 0.6 to 7.4 +/- 0.5 microns (p less than 0.005; WKY, 7.4 +/- 0.4 microns), and 4) a restoration of coronary vasodilator response to adenosine from 12.3 +/- 0.9 to 26.0 +/- 1.4 ml/min/g (p less than 0.005; WKY, 21.8 +/- 2.2 ml/min/g). Thus, in SHR with LVH and adverse structural remodeling of the cardiac interstitium, lisinopril reversed fibrous tissue accumulation and medial thickening of intramyocardial coronary arteries and restored myocardial stiffness and coronary vascular reserve to normal. CONCLUSIONS. These cardioreparative properties of angiotensin converting enzyme inhibition may be valuable in reversing left ventricular dysfunction in hypertensive heart disease.     

Effect of endurance exercise training on left ventricular size and remodeling in older adults with hypertension

BACKGROUND: It is not known whether exercise training can induce a reduction of blood pressure (BP) and a regression of left ventricular hypertrophy (LVH) in older hypertensive subjects. This study was designed to determine whether endurance exercise training, by lowering BP, can induce regression of LVH and left ventricular (LV) concentric remodeling in older hypertensive adults. METHODS: We studied 11 older adults with mild to moderate hypertension (BP 152.0 +/- 2.5/91.3 +/- 1.5 mm Hg, mean +/- SE), 65.5 +/- 1.2 years old, who exercised for 6.8 +/- 3.8 months. Seven sedentary hypertensive (BP 153 +/- 3/89 +/- 2 mm Hg) subjects, 68.5 +/- 1 years old, served as controls. LV size and geometry and function were assessed with the use of two-dimensional echocardiography. RESULTS: Exercise training increased aerobic power by 16% (p < .001), and it decreased systolic (p < .05) and diastolic (p < .05) BP, LV wall thickness (from 12.8 +/- 0.4 mm to 11.3 +/- 0.3 mm; p < .05), and the wall thickness-to-radius (h/r) ratio (from 0.48 +/- 0.02 to 0.41 +/- 0.01; p < .05). There were no significant changes in the controls. The changes in LV mass index (deltaLVMI) were different between the two groups. LV mass index decreased in the exercise group (deltaLVMI - 14.3 +/- 3.3 g) but not in the controls (deltaLVMI 1.4 +/- 4.1 g; p = .009). A multiple stepwise regression analysis showed that among clinical and physiological variables including changes in resting systolic BP, aerobic power, body mass index, and systolic BP during submaximal and maximal exercise, only the reduction in resting systolic BP correlated significantly with a regression of concentric remodeling (delta h/r ratio r = .80; p = .003). The other variables did not add to the ability of the model to predict changes in the h/r ratio. CONCLUSIONS: The data suggest that exercise training can reduce BP and induce partial regression of LVH and LV concentric remodeling in older adults with mild or moderate hypertension.     

原发性高血压患者颈动脉重构与左心室肥厚的关系

目的探讨原发性高血压(EH)患者颈动脉重构与左心室肥厚(LVH)的关系。方法筛选原发性高血压患者60例,正常对照组30例,经心脏及颈动脉超声检查,分别测算左心室质量指数(LVMI)、颈总动脉内膜-中层厚度(CCA-IMT)、斑块及两侧颈总动脉内径、扩张性(CD)、顺应性(CC)。EH组分为LVMI正常组及LVMI增高组。所测得的各组数据进行统计分析。结果EH组CCA-IMT高于对照组,LVMI增高组最高;EH组颈总动脉CC和CD较对照组均低;EH组中LVMI增高组斑块检出率及严重程度最高,LVMI正常组次之,均高于正常对照组。结论EH颈动脉重构与LVH存在相关性,颈动脉重构发生早于LVH的发生。     

急性心肌梗死后螺内酯干预对左室重构的影响

目的　探讨急性心肌梗死(AMI)患者应用螺内酯干预对于左室重构(LVRM)的影响。方法　4家医院共入选AMI患者88例,采用多中心、随机、对照的方法,对46例AMI患者在常规治疗的基础上加用螺内酯40mg/d(螺内酯组),对照组(n=42)常规治疗。在6个月干预期内检测两组血清Ⅲ型前胶原氨基端肽(PⅢNP)、脑钠肽(BNP)及超声心动图,以评价左室纤维化、左室功能和左室容积。结果　88例中,急性前壁心肌梗死患者43例,螺内酯组23例、对照组20例;急性下壁心肌梗死患者45例,螺内酯组23例、对照组22例。急性前壁心肌梗死组在治疗3、6个月时螺内酯组与对照组相比,血清PⅢNP和BNP明显降低[PⅢNP分别为( 260 .2±59. 9 )ng/L比( 328 .0±70 .3 )ng/L, P=0 .001, ( 197 .1±46 .3 )ng/L比( 266. 7±52 .4 )ng/L, P<0. 001 ,BNP分别为( 347 .4±84 .0)ng/L比(430 .1±62 .9)ng/L, P<0 .001, (243 .7±79. 7)ng/L比(334. 6±62. 8)ng/L, P<0. 001]。治疗6个月时螺内酯组较对照组左室舒张末期内径、左室收缩末期内径明显降低[分别为(51. 0±5 .5)mm比(55. 6±4 .5)mm, P=0 .005, (35 .7±4 .6)mm比(39 .1±5 .6)mm, P=0 .046]。急性下壁心肌梗死组在治疗6个月时螺内酯组与对照组相比血清PⅢNP、BNP水平无统计学意义,(P>0 05),并且左     

Attenuated coronary flow reserve and vascular remodeling in patients with hypertension and left ventricular hypertrophy

OBJECTIVES: The purpose of this study was to evaluate the association between hypertension and left ventricular hypertrophy (LVH) with both coronary vascular remodeling and endothelial function. BACKGROUND: The association between endothelial and nonendothelial coronary flow reserve with vascular remodeling in patients with hypertension and LVH is still unclear. METHODS: One hundred and eleven patients with normal or mildly diseased coronary arteries at angiography underwent intravascular ultrasound examination of the left anterior descending coronary artery. Patients were divided into three groups: group 1: n = 13, hypertensive patients with LVH; group 2: n = 30, hypertensive patients without LVH; group 3: n = 68, normotensive patients. Vessel and lumen area and atherosclerotic plaque area were evaluated. Vascular reactivity was examined using intracoronary adenosine and acetylcholine. RESULTS: Vessel area in group 1 (with LVH) was significantly (p < 0.01) greater than that in group 2 (without LVH), whereas, vessel area in both groups 1 and 3 was similar (12.8 +/- 0.8 mm2, 10.7 +/- 0.4 mm2 and 11.5 +/- 0.3 mm2). Coronary blood flow at baseline for patients in group 1 (with LVH) was significantly greater than it was for patients in groups 2 and 3 (81.1 +/- 9.9 ml/min, 56.5 +/- 6.2 ml/min and 48.1 +/- 3.2 ml/min, both p < 0.05). In comparison with groups 2 and 3, the response to both acetylcholine and adenosine was significantly impaired in patients with LVH. CONCLUSIONS: The current study demonstrates that hypertension with LVH is associated with both coronary vascular remodeling and attenuated endothelial and nonendothelial coronary flow reserve.