老年高血压患者动脉僵硬度与左心室肥厚关系

目的探讨老年高血压患者动脉僵硬度与左心室肥厚的关系。方法选择原发性老年高血压患者68例,以左心室重量指数(LVMI)作为评价左心室肥厚指标,将患者分为左心室肥厚组(32例)和非左心室肥厚组(36例)。以颈动脉-股动脉肢体动脉搏动波(cfPWV)和脉压作为评价动脉僵硬度指标,进行24 h动态血压监测、cfPWV及超声心动图检测,并进行多因素相关分析。结果左心室肥厚组较非左心室肥厚组患者cfPWV高[(14.45±1.83)m/s vs(10.89±1.94)m/s]、脉压大[(78.66±9.05)mm Hg(1 mm Hg=0.133 kPa)vs(60.39±7.74)mm Hg],两组比较,差异有统计学意义(P<0.01),logistic回归分析显示,LVMI与cfPWV、脉压呈正相关。结论动脉僵硬度增加是老年高血压患者左心室肥厚的重要危险因素。     

动态脉压对老年高血压患者靶器官损害的影响

目的探讨动态脉压对老年高血压患者靶器官损害的影响。方法选择原发性高血压患者146例,按24 h平均脉压(MPP)分为2组:24 h MPP≥60 mm Hg(1 mm Hg=0.133 kPa)为A组(60例),24 h MPP<60 mm Hg为B组(86例);另选健康体检者为对照组(C组,30例)。所有患者均行血清肌酐、动态血压、超声心动图、颈动脉超声检查;计算肌酐清除率(Ccr)、24 h平均收缩压(MSBP)、24 h平均舒张压、24 h MPP、左心室重量指数(LVMI)、LVEF、颈动脉内膜中层厚度(IMT)。结果与C组比较,A组和B组患者24 h MSBP、24 h MPP、LVMI、IMT、左心室肥厚、左心室功能受损、脑损害、肾功能受损、颈动脉斑块发生率明显升高,Ccr、LVEF水平明显降低(P<0.05,P<0.01);与B组比较,A组患者Ccr、LVEF水平明显降低,24 h MSBP、24 h MPP、LVMI、IMT、靶器官损害发生率均明显升高(P<0.05,P<0.01)。24 h MPP与心脑肾和颈动脉损害相关(P<0.05)。结论动态脉压增大与老年高血压患者靶器官结构和功能的损害相关;动态脉压越大,靶器官损害越严重。     

老年高血压患者血压变异性与靶器官损害的关系

目的探讨老年高血压患者血压变异性(BPV)与靶器官损害的关系。方法选择133例老年人群临床资料,分为高血压组98例和对照组35例,进行24 h动态血压监测,比较2组24 h、昼间、夜间收缩压和舒张压的平均值及标准差,以标准差代表BPV的值。根据昼间收缩压标准差的第50百分位数将高血压组分为昼间高BPV组48例和昼间低BPV组50例,比较2组的危险因素、颈总动脉内膜中层厚度(IMT)、左心室重量指数(LVMI)和微量白蛋白尿。结果高血压组24 h、昼间、夜间收缩压和收缩压变异性明显高于对照组(P<0.05,P<0.01);昼间高BPV组IMT、LVMI明显高于昼间低BPV组[(1.09±0.44)mm vs(0.94±0.17)mm,P<0.05;(239.97±52.87)g/m~2 vs(208.41±46.10)g/m~2,P<0.01]。多元线性回归分析显示,昼间收缩压变异性与颈总动脉IMT、LVMI独立相关。结论老年高血压患者BPV较高,昼间收缩压变异性是颈总动脉IMT增厚和左心室肥厚的预测指标。     

老老年人群动态血压参数与动脉僵硬度的相关性

目的探讨老老年人群动态血压参数与动脉僵硬度的相关性。方法筛选年龄≥80岁的老老年人238例,以血压≥160/95 mm Hg(1 mm Hg=0.133 kPa)为标准,分为高血压组(134例)和对照组(104例),并进行臂-踝脉搏传导速度(baPWV)和24 h动态血压监测。用Pearson分析动态血压各参数与动脉僵硬度的相关性。结果高血压组baPWV高于对照组(P<0.05)。高血压组偶测收缩压,24 h、昼间和夜间收缩压、舒张压、脉压,收缩压负荷及舒张压负荷均高于对照组.夜间收缩压下降率、舒张压下降率低于对照组,差异有统计学意义(P<0.05,P<0.01)。baPWV与偶测血压;24 h收缩压、舒张压、脉压;昼间收缩压、舒张压、脉压、心率;夜间收缩压、舒张压、脉压;收缩压负荷、舒张压负荷呈正相关(P<0.05,P<0.01),而与夜间收缩压下降率呈负相关(P<0.01)。结论高血压是老老年人群动脉僵硬度增加的一个重要因素,动脉僵硬度与动态血压、脉压、心率及血压负荷相关。     

老年高血压和糖尿病患者动脉僵硬度的影响因素分析

目的 评价老年高血压和(或)糖尿病患者动脉僵硬度及其影响因素. 方法 320例老年患者分为4组:对照组、糖尿病组、高血压组、高血压并存糖尿病组(联合患病组).收集年龄、体质指数、性别、吸烟、血压、脉压及平均动脉压,测定血清空腹血糖、血脂、糖化血红蛋白、超敏C反应蛋白等;并应用COLIN-VP1000动脉硬化测定仪测量入选者踝臂脉搏波传导速度(baPWV)以评价对动脉硬化的影响. 结果 联合患病组、糖尿病组、高血压组、对照组baPWV值分别为(2165.9±479.9)cm/s、(2158.6±386.9)cm/s、(1881.2±383.8)cm/s和(1667.2±279.3)cm/s,联合患病组、高血压组及糖尿病组的baPWV水平与对照组比较,差异均有统计学意义(F=8.473,P＜0.05),联合患病组与糖尿病组的baPWV值比较,差异无统计学意义,高血压组与糖尿病组及联合患病组的baPWV值比较,差异有统计学意义(均P＜0.05).联合患病组脉压、超敏C反应蛋白最高,与对照组比较,差异有统计学意义(均P＜0.05).多元线性回归分析结果显示,血清空腹血糖、平均动脉压、脉压、超敏C反应蛋白、低密度脂蛋白胆固醇与baPWV水平呈正相关(均P＜0.05). 结论 糖尿病、高血压是老年人动脉僵硬度增高的影响因素,而高血糖对老年人动脉僵硬度的影响可能起了更重要的作用.血糖、平均动脉压、脉压、超每C反应蛋白、低密度脂蛋白胆固醇均是影响动脉僵硬度的独立危险因素.     

原发性高血压患者动态脉压、年龄与靶器官损害的关系

目的 探讨原发性高血压患者24h收缩压、舒张压及脉压变化与靶器官损害的关系。方法 对296例观察对象进行24h动态血压监测，其中血压正常组92例，单纯血压升高的原发性高血压患者为原发性高血压组86例，原发性高血压伴靶器官损害患者为伴靶器官损害组118例。296例根据动态平均脉压水平分为3个亚组（脉压〈40mmHg组、40mmHg≤脉压〈50mmHg组、脉压≥50mmHg组），对比分析24h动态血压监测各指标。将伴靶器官损害组按年龄分为〈60岁、≥60岁2个亚组，观察对比24h动态血压监测各指标的变化。结果 （1）伴靶器官损害组24h收缩压、白昼舒张压、夜间舒张压低于原发性高血压组（P〈0．01）；（2）随高血压患者病变程度的加重，脉压也随之增大（P〈0．01），依次为伴靶器官损害组、原发性高血压组和血压正常组；（3）伴靶器官损害组两年龄间脉压差异无统计学意义（P〉0．05）。结论 动态脉压的变化可以反映高血压患者病变程度，舒张压低及动态脉压增大是原发性高血压伴靶器官损害患者动态血压变化特点之一。     

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。     

高龄老年高血压患者夜间血压与靶器官损害相关性研究

目的 探讨高龄老年高血压患者夜间血压控制水平与靶器官损害之间的关系及其干预策略。方法2005年1月至2007年12月仁济医院老年病科就诊208例高龄老年高血压患者（年龄≥80岁）,根据动念血压检测结果分为单纯夜间血压控制不良组（n=102）和全天血压控制均在正常范围组（n=106）,对患者的临床资料、生化指标、心脏彩超和颈动脉B超榆查结果及降压治疗方案进行分析。结果两组年龄、性别、血肌酐、血尿素氮、尿酸水平的差异均无统计学意义。两组总胆同醇、甘油三酯、空腹血糖、左室相关参数、颈动脉结构血流参数及斑块情况的差异有统计学意义（P〈0．05）;CCB＋ACEI／ARB组合比利尿剂＋ACEI／ARB组合,在高龄老年高血压患者夜间血压水平控制方面更为有效（JP〈0．001）结论高龄老年高血压患者夜间血压水平与左心室肥厚、颈动脉斑块（P〈0．05）正相关;CCB＋ACEI／ARB药物组合在高龄老年高血压患者夜间血压水平控制效果较好。     

基质金属蛋白酶与老年高血压患者左心室肥厚的相关性

目的通过测定老年高血压患者血清基质金属蛋白酶1(MMP-1)、MMP-9、基质金属蛋白酶抑制剂1(TIMP-1)水平与左心室后壁厚度(LVPWT)、左心室质量指数(LVMI),探讨基质金属蛋白酶在老年人高血压心室重构中的作用。方法 60岁以上老年高血压患者89例,根据有无左心室肥厚分为两组,高血压合并左心室肥厚32例,高血压无左心室肥厚57例,另52名健康老年人设为对照组超声心动图测LVPWT及LVMI。酶联免疫吸附法(ELISA)测定血清MMP-1、TIMP-1水平。结果健康对照组、高血压无左心室肥厚组、高血压合并左心室肥厚组LVPWT、LVMI、TIMP-1和MMP-9水平逐渐升高(均为P<0.05),而血清MMP-1水平逐渐降低(均为P<0.05)。LVMI、LVPWT与血清MMP-9、TIMP-1水平呈正相关(均为P<0.05),与MMP-1水平呈负相关(均为P<0.05)。结论 MMP-9水平与左心室质量、左心室壁厚度呈正相关,而MMP-1水平与之呈负相关。细胞外基质重构可能与老年高血压有关。     

高血压病患者左心室向心性肥厚与颈动脉僵硬度的相关性研究

[摘 要] 目的 研究高血压患者颈动脉硬化与左心室向心性肥厚之间的相关性。方法 回顾性分析303例高血压患者作为研究对象,90例同龄健康自愿者作为对照组。患者进行超声心动图和颈动脉超声高分辨率回声跟踪检查。基于左心室质量指数(left ventricular mass index,LVMI)和相对壁厚(relative wall thickness,RWT)将高血压患者分成四个小组：正常几何构型(normal geometry,N, 57例), 向心性重构（concentric remodeling,CR, 48例),向心性肥厚(concentric hypertrophy, CH, 62例)和偏心肥厚(eccentric hypertrophy,EH,35例)。基于β硬化度（β）、杨氏弹性模量(Young elastic modulus,Ep)、动脉动脉顺应性(arterial compliance,AC)、单点脉搏波速度(one-point pulse wave velocity,PWVβ)和波反射增强指数(wave reflection augmentation index,AI)对患者左心室内中膜复合体壁厚度(Intima-media thickness,IMT)和动脉硬化度进行评估。结果 单变量分析结果显示β-硬化度> 8.4、杨氏弹性模量Ep > 136 kPa、局部单点脉搏波速度-β> 7.1 m / s、增加指数AI > 21.9%、收缩压> 151 mm Hg、脉压 > 54、IMT > 0.56及糖尿病与向心性肥厚显著相关。然而,多变量分析结果显示只有增加指数AI（OR=3.64,p = 0.04）,局部单点脉搏波速度-β> 7.1 m/s（OR=2.82,p = 0.013）,收缩压（OR=3.11,p = 0036）及糖尿病（OR=3.73,p = 0.007）与患者向心性肥厚独立相关。结论 高血压患者向心性肥厚与颈动脉硬化及波反射增强指数显著相关,而与收缩压和糖尿病独立相关。     

高龄高血压病患者昼夜血压节律对左心室肥厚和左心室功能的影响

目的　观察高龄高血压病患者昼夜血压节律对左心室肥厚和左心室功能的影响。方法　根据夜间血压下降率将 6 8例年龄≥ 80岁的高血压病患者分为非杓型组和杓型组 ,应用 2 4h动态血压监测和超声心动图观察并比较高血压病患者的动态血压节律以及左心室结构和功能的特点。结果　非杓型组 2 4h收缩压、2 4h舒张压、夜间收缩压、夜间舒张压明显高于杓型组。非杓型组较杓型组左心室重量及左心室重量指数明显增加 ,舒张早期血流 (E波 )的峰值流速减慢 ;心房收缩期血流的峰值流速增大 ;心房收缩期血流的峰值流速 舒张早期血流的峰值流速比值加大。结论　非杓型血压节律的高龄高血压病患者较杓型血压节律者的左心室肥厚和左心室舒张功能减退发生率更高     

Association between left ventricular hypertrophy and changes in arterial stiffness during hypertensive treatment

Cardio-ankle vascular index (CAVI) has been demonstrated as a parameter of arterial stiffness, which antihypertensive therapy may improve. However, little information is available about the factors affecting changes in arterial stiffness assessed by CAVI during antihypertensive therapy. We performed a study to examine the factors affecting changes in arterial stiffness assessed by CAVI during antihypertensive therapy. Eighty treated hypertensive patients (71?±?10 years) were divided into two groups: 50 patients showing a decrease in CAVI (Group 1) and 30 patients showing an increase (Group 2) during observation (24?±?11 months) of antihypertensive therapy. The groups did not differ in the rates of use of angiotensin II receptor blockers or calcium channel blockers. Age (Group 1: 67?±?11 versus Group 2: 74?±?8 years), left ventricular mass index (LVMI) (Group 1: 103?±?19 versus Group 2: 120?±?24?g/m²) and systolic blood pressure (Group 1: 133?±?17 versus Group 2: 144?±?23?mm?Hg) at the start of observation were significantly higher in Group 2 than in Group 1 (p?=?0.003, p?=?0.001 and p?=?0.027, respectively). The changes in CAVI during observation were correlated only with LVMI (r?=?0.289, p?=?0.009) at the start of observation for all 80 patients. It may be difficult to improve arterial stiffness assessed by CAVI during antihypertensive therapy in hypertensive patients with left ventricular hypertrophy.     

Left ventricular hypertrophy regression and function changes with ketanserin in elderly hypertensives

Summary Ketanserin is a serotonin antagonist with age-related antihypertensive efficacy. Its effects on left ventricular (LV) function and hypertrophy have not been adequately reported. We studied noninvasively 54 elderly hypertensives before and 6 months after ketanserin monotherapy. Mean blood pressure was controlled (174/101 to 145/86 mmHg, p<0.0001) with no heart rate changes. LV dimensions and volumes remained unchanged, as did all LV ejection indices, thus preserving LV output (p=ns). Total peripheral resistances fell (from means of 1986 to 1615 dynes, cm.s^-5, p<0.0001), as did LV systolic wall stresses. Mean LV mass was reduced (248 to 237 g, p<0.0001), mainly due to interventricular septum thinning (11.8 to 11.1 mm, p<0.0001), resulting in a decrease in mean LV cross-sectional area (21.3 to 20.5 cm², p<0.0001) and mass/volume ratio (2.14 to 2.01 p=0.0001). Thus, LV hypertrophy regression did not affect contractility (LV mass index relation to stress/end-systolic volume index, r=–0.558 before and r=–0.564 after ketanserin therapy). It is concluded that ketanserin is an effective antihypertensive agent in the elderly that reduces LV hypertrophy indices and maintains cardiac output, with no concomitant burdening on LV hemodynamics.     

Relationship between left ventricular geometric pattern and systolic and diastolic function in treated Nigerian hypertensives

Introduction

Despite a high worldwide prevalence of left ventricular hypertrophy among black patients, the association of a specific left ventricular geometric pattern with left ventricular dysfunction is rare. The aim of this study was to explore the possibility of such an association in Nigerian hypertensives.

Methods

This was a retrospective study consisting of 188 treated hypertensives. Echocardiography was used to allocate the patients to the following four groups: normal geometric pattern, concentric remodelling, eccentric hypertrophy and concentric hypertrophy.

Results

The mean age of the study population was 55.95 ± 10.71 years. There were 75 females (39.9%). Concentric hypertrophy occurred in 72 (38.3%) patients and concentric remodelling in 53 (28.2%). Only 30 (16%) had a normal left ventricular geometric pattern. Hypertensive subjects with eccentric hypertrophy had the lowest ejection fraction, fractional fibre shortening and left ventricular ejection time but these did not reach statistical significance. The mean left atrial dimension was highest in the subjects with eccentric hypertrophy.

Conclusion

In this study population of treated Nigerian hypertensives, concentric remodelling and hypertrophy were the predominant left ventricular geometrical patterns.