左旋氨氯地平治疗高血压左心室肥厚38例疗效分析

高血压所致的左室肥厚 (LVH)是心血管事件的一项独立危险因子 ,有IVH的高血压病人罹患室性心律失常和猝死的危险性显著增加 ,其心血管病病死率较无LVH者增加 8倍[1] 。本文应用钙通道阻滞剂左旋氨氯地平治疗高血压左心室肥厚病人 38例 ,取得较好的疗效 ,现报告如下 :1　对象和方法1 1　对象 :38例均为本院门诊或住院病人 ,原发性高血压 (EH)诊断符合 1999年 10月《中国高血压防治指南》(试行本 )诊断标准 ,并经超声心动图检查确诊为LVH。其中男 2 5例 ,女 13例 ,年龄 4 5～ 76岁 ,平均年龄 6 0± 10岁。排除继发性高血压及其他心脏疾…     

左旋氨氯地平对原发性高血压患者左心室肥厚的逆转作用

高血压(EH)患者常出现左心室肥厚(LVH),LVH逆转与患者的预后有关。2004年3月~2005年9月,我们观察了左旋氨氯地平对EH患者的降压疗效及其对LVH的逆转作用。现报告如下。临床资料:EH患者60例,男40例,女20例;年龄30~70岁。符合1999年WHO/ISH制定的高血压诊断标准,即在未服抗高血压     

高血压合并左心室肥厚患者血管内皮舒张功能与尿酸的关系

目的探讨高血压合并左心室肥厚(LVH)患者的血流介导的内皮依赖性血管舒张功能(FMD)与尿酸的关系。方法选择2006-08-2011-02福建医科大学附属第一医院门诊轻中、度高血压患者277例(包括未降压治疗和已接受降压治疗的患者),男159例,女118例,年龄(58.5±11.0)岁。根据左心室质量指数(LVMI)≥125(男)或≥110g/m2(女)分为高血压合并LVH组(LVH组,n=83)与高血压无LVH组(non-LVH组,n=194);选择同期未服用任何药物在我院门诊初诊的体检正常的非高血压患者41例作为对照组。采用超声心动图法测定LVMI;采用高分辨超声技术测定反应性充血前后肱动脉内径的变化率,作为肱动脉FMD。采用氧化酶法测定空腹尿酸。结果与对照组比较,non-LVH组和LVH组FMD均减退[(7.3±3.5)%,(5.7±2.2)%比(9.9±3.1)%,P<0.05],高尿酸血症(HUA)发生率明显升高(39.2%,40.1%比17.1%,P<0.05)。高血压患者中,HUA与尿酸正常患者比较,FMD减弱[(6.3±2.5)%比(7.1±3.6)%,P<0.05];进一步的亚组分析发现,non-LVH组HUA与尿酸正常者比较,FMD减弱[(6.5±1.9)%比(7.7±2.6)%,P<0.05],但LVH组HUA与尿酸正常患者的FMD差异无统计学意义。相关分析显示FMD与尿酸呈负相关(r=-0.18,P<0.05)。结论尿酸与血管内皮功能相关,已有LVH的高血压患者,尿酸对血管内皮功能进一步影响不明显。     

左旋氨氯地平对自发性高血压大鼠内皮功能的保护作用

目的 探讨左旋氨氯地平对自发性高血压大鼠(SHR)内皮依赖性舒张功能的影响.方法 20只SHR随机分为左旋氨氯地平治疗组(SHR-A组)和高血压对照组(SHR-C组),同周龄WKY大鼠作为正常对照组(WKY组).左旋氨氯地平治疗12周后,检测各组大鼠胸主动脉对乙酰胆碱(ACh)和硝普钠(SNP)的舒张反应,以及血清NO、内皮素(ET)和超氧化物歧化酶(SOD)的水平.结果 与SHR-C组相比,SHR-A组胸主动脉环对ACh的最大舒张反应明显增强(P<0.01).左旋硝基精氨酸甲酯能够消除两组之间的差异.3组大鼠胸主动脉环对SNP的最大舒张反应无统计学意义(P>0.05).SHR-A组与SHR-C组、WKY组比较血清NO、SOD浓度明显增加,而血浆ET水平显著降低(P<0.05).结论 左旋氨氯地平干预能够显著改善SHR血管内皮依赖性舒张功能,其作用机制可能与增加内皮NO的合成和释放有关.     

高血压与左心室肥厚

左心室肥厚 ( LVH)是心血管疾病的重要危险因素 ,高血压是 LVH最常见的原因。本文就高血压患者 LVH的诊断方法、致病因素、病理生理、不良后果及药物治疗等问题作介绍     

马来酸左旋氨氯地平对原发性高血压患者血压变异性及左心室肥厚的影响

目的观察马来酸左旋氨氯地平对高血压患者血压、血压变异性及左心室肥厚的影响。方法 150例原发性高血压合并左心室肥厚患者作为试验组,停药2周后,用马来酸左旋氨氯地平治疗24周;同时选取50例原发性高血压患者作为对照组,服用硝苯地平24周。采用无创性携带式动态血压监测仪监测动态血压、血压变异性及测定治疗前后左心室肥厚指标。结果两组治疗前后血压比较,差异均无统计学意义(P>0.05)。两组治疗后左心室各项指标,左心室舒张末期容积(LVDd)、舒张末期厚度(IVSd)、左心室后壁舒张末期厚度(LVPWd)、左心室重量指数(LVMI)比较,差异有统计学意义(P<0.05)。结论原发性高血压患者血压变异性增高,合并出现左心室肥厚,马来酸左旋氨氯地平在稳定降压的同时可降低血压变异性,逆转高血压左心室肥厚。     

老年高血压患者左心室肥厚与心功能的关系

老年高血压患者因病史较长 ,多容易出现左心室肥厚 ,本研究旨在探讨老年高血压患者左心室肥厚与心功能的关系。1　对象与方法为本院干部病房 2 0 0 0年 6月～ 2 0 0 2年 5月住院治疗的高血压患者 1 5 3例 ,男 1 34例 ,女 1 9例 ,年龄 69～ 91 (平均 77.4)岁。高血压诊断以 1 999年1 0月的中国高血压防治指南为标准 ,即收缩压 1 40mmHg( 1mmHg =0 .1 33kPa)和 (或 )舒张压≥ 90mmHg。因冠心病或肺心病入院治疗而同时并发高血压的患者不包括在此研究病例中。所有高血压患者入院后 ,常规进行二维超声心动图的检查。采用美国ATL80 0型彩色显…     

高血压左心室肥厚与脑卒中关系的研究

高血压引起的左心室肥厚(LVH)是多种心血管疾病如冠心病、心肌梗死、心力衰竭的独立危险因素,它与脑卒中的关系也非常密切,进一步研究两者之间的关系对研究脑卒中的发病机制、治疗和预防具有重要意义.     

原发性高血压左心室肥厚患者纤溶功能的变化

目的 了解高血压左心室肥厚(LVH)患者血清溶栓功能指标的变化情况及其临床意义. 方法 对40例LVH患者血清P选择素(Ps)、组织型纤溶酶原激活物(tPA)、纤溶酶原激活物抑制物(PAI)和血管性血友病因子(vWF)水平进行检测,并与30例健康体检者和45例高血压非左心室肥厚者(NLVH)比较. 结果 LVH组血清Ps[(38.3±11.63)Pg/L]、PAI[(1.5±0.6)Au/mL]和vWF[(187.3±56.6)%]高于NLVH组[Ps(31.7±10.6)pg/L、PAI(0.8±0.3)Au/mL、vWF(127.8±36.4)%],NLVH组上述指标又高于对照组[Ps(22.5±12.4)pg/L、PAI(0.6±0.3)Au/mL、vWF(98.5±34.8)%](P＜0.01);tPA水平分别为:LVH组(0.3±0.3)、NLVH组(0.7±0.4)、对照组(1.0±0.5)μg/L,LVH组tPA低于NLVH组,NI,VH组又低于对照组(P＜0.01). 结论 原发性高血压LVH患者的抗凝作用减弱、血小板黏附与聚集以及纤溶活性下降,这些变化可能与此病常见的并发心脑血管意外的发生与发展有关.     

一氧化氮和内皮素在高血压左室肥厚形成中的作用

目的 探讨一氧化氮（NO）和内皮素（ET）在高血压左室肥厚（LVH）形成中的作用。方法 采用放射免疫分析法（RIA）和硝酸还原酶法检测30例单纯原发性高血压（EH,观察Ⅰ组）、30名健康体检者（对照组）及20例EH伴LVH（观察Ⅱ组）患者降压治疗前后血清ET、NO水平。并对结果进行相关分析。结果 观察Ⅰ组血清ET明显高于对照组、NO明显低于对照组（P均〈0．01）;观察Ⅱ组血清ET明显高于观察Ⅰ组、NO明显低于观察Ⅰ组（P均〈0．01）,且ET与NO水平呈负相关（r=0．586,P〈0．01）;左心室重量指数（LVMI）与ET呈正相关（r=0．427,P〈0．05）、与NO呈负相关（r=0．653,P〈0．01）。观察Ⅱ组治疗后,血清ET水平明显低于治疗前、NO水平明显高于治疗前（p均〈0．01）。结论 ET和NO两者失衡可能参与了EH及LVH形成的病理生理过程。     

脉压对老年高血压病患者左心室肥厚的影响

目的　比较动态脉压和诊所脉压对老年高血压病患者左心室肥厚的影响。方法　选择初诊的轻 中度高血压病患者 118例。所有入选病例测量非同日 3次诊所血压、进行 2 4h动态血压监测和超声心动图检查。根据动态脉压和诊所脉压水平各分为 3组 ,并分别比较。结果　动态脉压与年龄、高血压病史、左心室重量指数、动脉僵硬度指数和体重指数呈显著的相关性。动脉僵硬度随分组脉压的增大呈显著递增 ,其与动态脉压的相关性明显强于诊所脉压。动态脉压与左心室重量指数的相关性明显强于诊所脉压。结论　脉压升高是老年高血压病患者左心室肥厚的重要危险因素 ,与诊所脉压比较 ,动态脉压更能反映高血压靶器官损害的程度。     

增益指数与原发性高血压左室肥厚及心脏功能相关性研究

目的探讨桡动脉增益指数(radial augmentation index,AIr)与原发性高血压患者左室肥厚和心脏功能的关系。方法前瞻性选取2009年1月至3月在北京大学第三医院心内科住院的患原发性高血压、超声心动图测定的左室射血分数(left ventricular ejection fraction,LVEF)≥50%的患者共102例,分析心率为75次/min标准化的桡动脉增益指数(AIrP75)和超声心动图测量的心脏结构及功能指标的关系。结果 102例患者中男性占68.6%,平均年龄(65.0±9.6)岁。AIrP75与心肌收缩期运动速度峰值(peakmyocardial systolic velocity,Sm)呈负相关(r=-0.24,P=0.017),与左室心肌重量指数(left ventricular massindex,LVMI)呈正相关(r=0.22,P=0.027)。将AIrP75与患者的临床特征及生化指标代入多元线性回归方程,结果显示AIrP75仍与LVMI(β=0.354,s=0.164,sβ=0.214,95%CI 0.028～0.681,P=0.034)及Sm(β=-0.042,s=0.020,sβ=-0.209,95%CI-0.082～-0.002,P=0.040)独立相关。结论本研究结果显示脉搏波增益指数(AIrP75)与左室射血分数正常的原发性高血压患者左室肥厚和心肌收缩功能受损独立相关,提示动脉僵硬度增加可能是原发性高血压患者心脏结构和(或)功能受损的早期标志。     

高血压左室肥厚的QT离散度及左室Tei指数的研究

目的探讨原发性高血压左室肥厚与QT离散度及左室Tei指数的关系。方法高血压病组109例(非左室肥厚组83例,左室肥厚组26例),正常组30例,测定QT离散度及左室Tei指数。结果高血压病组无论有无左室肥厚,其QT离散度及左室Tei指数均显著大于正常组(QTd:43.9±15.1ms,69.2±16.9msvs36.2±11.3ms,p<0.05;Tei指数:0.54±0.06,0.60±0.14vs0.38±0.07,p<0.05)。高血压病左室肥厚组的左室Tei指数及QT离散度较非左室肥厚组有增大的趋势(QTd:69.2±16.4msvs43.9±15.1ms,p<0.05;Tei指数:0.60±0.14vs0.54±0.06,p>0.05)。结论高血压左室肥厚时,QT离散度及左室Tei指数增大,表明高血压左室肥厚可导致QT离散度增大及左室舒张功能不全。     

比索洛尔与卡维地洛对原发性高血压疗效及逆转左心室肥厚的对比研究

目的对比研究富马酸比索洛尔和卡维地洛治疗原发性高血压的疗效以及逆转左心室肥厚的作用。方法将106例原发性高血压伴左心室肥厚的患者随机分为富马酸比索洛尔组(49例)和卡维地洛组(46例),于服药前及服药后3、6及12个月分别监测两组患者血压、心率,并测定左心室舒张末内径、舒张期室间隔厚度、左心室后壁厚度、左心室射血分数、心排血量、A峰速度、E峰速度及A峰与E峰比值(A/E比值)。结果两组治疗后心率比治疗前减慢,差异有统计学意义(P0.05);富马酸比索洛尔组治疗后心率低于卡维地洛组,差异有统计学意义(P0.05)。两组治疗后随访3、6、9个月的血压均比治疗前降低,差异有统计学意义(P0.05)。两组治疗前后左心室射血分数、心排血量比较,差异无统计学意义(P0.05);两组治疗后A/E比值均比治疗前明显降低。两组左心室质量指数、左心室舒张末内径、舒张期室间隔厚度、左心室后壁厚度治疗后均比治疗前降低,差异有统计学意义(P0.05);富马酸比索洛尔组治疗后上述指标比卡维地洛组低,差异有统计学意义(P0.05)。结论富马酸比索洛尔和卡维地洛在降低血压的同时,均能改善左心室舒张功能,并明显减轻左心室肥厚;富马酸比索洛尔比卡维地洛减轻左心室肥厚效果更强,并可以有效控制心率。     

替米沙坦改善原发性高血压病患者心肌肥厚及早期肾功能失调

目的:评估替米沙坦在高血压病靶器官损害中的保护作用。方法:轻中度原发性高血压病左室肥厚患者60例服用替米沙坦40～80mg/d,共26周,服药前后行超声心动图,观察舒张末期室间隔厚度（IVST）,舒张末期左心室后壁厚度（LVPWT）及A/E比值的变化;并计算左室心肌质量指数（LVMI）的改变;同时放射免疫分析法测量血β2微球蛋白（β2MG）、尿β2MG含量。结果:替米沙坦能有效降低血压,降压有效率为72%,治疗后LVMI降低（146±12vs123±10）（P<0.01）,A/E值改善（P<0.05）,血、尿β2MG水平降低。结论:替米沙坦在降低血压同时能够有效地保护心肾功能。     

缬沙坦对原发性高血压左心室肥厚及舒张功能的影响

目的 评价缬沙坦对高血压患者左心室肥厚及左心室舒张功能的影响。方法 选原发性高血压并左心室肥厚患者48例,随机分为缬沙坦治疗组和硝苯地平缓释片治疗组（对照组）,治疗6个月,控制收缩期血压低于或等于140 mm Hg（1mm Hg=0.133kPa）,舒张期血压低于或等于95 mm Hg。于治疗前、治疗3个月、6个月作体格检查、血生化及心脏超声检查,记录心率、收缩压、舒张压、左心室舒张末期内径、室间隔厚度、左心室后壁厚度、左心室射血分数、舒张早期和晚期最大速度比值（E/A比值）,计算左心室重量指数。结果 调整用药后两组患者血压均达目标值;治疗3个月后两组病人左心室重量指数和E／A即显示差异,但缺乏统计学意义;治疗6个月后缬沙坦治疗组的左心室重量指数和E／A比值较对照组改善明显,而两组治疗前后左心室射血分数均无明显变化。结论 相对于硝苯地平缓释片,缬沙坦对于原发性高血压患者的左心室肥厚和左心室舒张功能有更明显的改善,这种受益是独立于其降压作用之外的。     

Modified Cornell electrocardiographic criteria in the assessment of left ventricular hypertrophy geometry of patients with essential hypertension

To evaluate the value of modified Cornell electrocardiographic criteria in the assessment of left ventricular hypertrophy (LVH) for patients with essential hypertension. A total of 381 patients with essential hypertension diagnosed in our hospital were selected. Using the left ventricle (LV) geometric patterns classified by the American Society of Echocardiography (ASE), we examined the distribution of the modified Cornell criteria of Ravl + S_D (the deepest S wave in 12‐lead ECG) in different geometric patterns and analyzed the correlation of modified Cornell criteria with changes in the LV geometric patterns using multiple linear regression analysis. The distribution of modified Cornell criteria, Sokolow‐Lyon criteria (RV5/V6 + SV1), and Cornell criteria (Ravl + SV3) in gender‐specific hypertensive geometric patterns were significantly different (P ≤ .01 for all). The voltage of Ravl + S_D in male patients showed an increase trend in the normal geometry (NG), concentric remodeling (CR), concentric hypertrophy (CH), and eccentric hypertrophy (EH) groups, and this increase trend was significantly in the unadjusted model and the adjusted model. The voltages of Ravl + SV3 and RV5/V6 + SV1 of male patients in CR, CH and RH groups showed a gradual increase trend, but the increase trend in CR group has no statistical significance compared to that in NG group (P ≥ .05). The voltages of Ravl + S_D, RV5/V6 + SV1, and Ravl + SV3 in female patients in CR, CH and EH groups showed a trend of increase after decrease in the adjusted model. In conclusion, the modified Cornell criteria could dynamically reflect left ventricular hypertensive geometry of male patients.     

Effects of bisoprolol on left ventricular hypertrophy in essential hypertension

Summary Previous studies have shown that beta-adrenergic blocking drugs can reverse ventricular hypertrophy in patients with systemic hypertension. Thirty patients with essential hypertension and left ventricular hypertrophy were studied at baseline after withdrawing all previous treatments and after 6 months of treatment with 5–20 mg of bisoprolol, a new beta-selective agent, to assess its possible action on left ventricular mass. Three patients did not finish the study. Blood pressure was reduced to below 160/90 mmHg in 22 of the remaining 27 patients. At the end of follow-up, the left ventricular mass (echocardiography) was reduced from 308.1±89 g to 262.3±51 g (p<0.001) and left ventricular mass index from 165±47.4 g/m² to 141.03±26.7 g/m² (p<0.001). The ratio of E wave/A wave velocity of transmitral blood flow measured by Doppler increased from 0.86±0.44 to 1.07±0.45 (p=0.005). Peak filling rate, derived from nuclear ventriculography, changed from 2.05±0.4 EDV/sec before the treatment to 2.23±0.47 EDV/sec after it (p=0.0046). Serum lipids as well as other biochemical tests were unchanged. Left ventricular volumes and ejection fraction did not change, and treadmill exercise time increased from 343±125 seconds to 420±135 seconds (p=0.002). Maximal systolic blood pressure during exercise decreased from 197.2±19.7 mmHg to 182.9±25.8 mmHg (p=0.011). There were few side effects. We conclude that bisoprolol reduces left ventricular mass, preserves systolic function, and improves diastolic function of the left ventricle in hypertensive subjects with left ventricular hypertrophy.     

Regression of left ventricular hypertrophy and systolic function in hypertensive patients during long-term treatment with ketanserin

Summary It is now generally accepted that antihypertensive therapy can induce regression of left ventricular hypertrophy (LVH) in hypertensive subjects. However, the influence of LVH reversal on both the systolic and diastolic functions, and particularly the ability of the heart to meet sudden overloads caused by exercise and/or recurrence of hypertension, remain unanswered questions. The long-term effects of ketanserin, a selective serotonin S₂-receptor antagonist with additional alpha₁-adrenergic blocking properties, on LVH and systolic function were studied in 13 untreated subjects (age range 35–55 years) with mild-to-moderate essential hypertension, echocardiographic evidence of LVH, and normal ejection fraction. Blood pressure values and echocardiographic measurements of dimensions, wall thicknesses, and indices of LV mass were determined before and after 3, 6, and 12 months treatment; ejection fractions at rest and during exercise were evaluated by equilibrium multigated radionucleide angiocardiography at baseline and after 12 months of therapy. Mean arterial pressure was significantly reduced from the first month of treatment (p<0.001) and remained well controlled up to the end of the trial. Both posterior and septum wall thicknesses decreased after 3 months of therapy and remained stable throughout the whole study period. LV mass index decreased from a mean ± SD of 187.7±47.6 g/m² to a mean of 157.81±31.63 g/m² (p<0.01) at the third month, reaching greater decreases after 6 months (156.05±31.00 g/m²) and after 12 months (153.21±28.80 g/m²) of treatment. A significant correlation was found between LV mass and posterior wall thickness at the different observation times in the study. Finally, the regression of LVH at the end of therapy was not associated with impairment of systolic function, as assessed by measurements of ejection fraction at rest and during exercise.