高同型半胱氨酸血症对老年原发性高血压患者动脉僵硬度的影响

目的 探讨高同型半胱氨酸血症(HHcy)对老年原发性高血压患者动脉僵硬度的影响。方法 选择老年原发性高血压患者66例(高血压组),其中HHcy 32例,非HHcy 34例。另外入选无高血压史老年健康体检者58例(对照组),其中HHcy 14例,非HHcy 44例。测定2组患者血脂、空腹血糖、空腹胰岛素及血同型半胱氨酸(Hcy)水平,计算稳态模型胰岛素抵抗指数。通过颈动脉-股动脉肢体动脉搏动波(cfPWV)评估动脉僵硬度。结果 高血压组Hcy和cfPWV显著高于对照组[(15.48±6.38)μmol/L vs(12.96±4.01)μmol/L,P0.05;(14.46±1.62)m/s vs(10.81±1.59)m/s,P0.05]。所有受试者血浆Hcy与cfPWV呈正相关(r=0.529,95%CI:0.040~0.079,P0.01)。高血压组HHcy患者胰岛素抵抗指数和cfPWV显著高于非HHcy患者[3.84±2.16 vs 2.58±1.56,P=0.018;(14.97±1.22)m/s vs(11.09±1.49)m/s,P=0.004]。结论 伴有HHcy的老年原发性高血压患者动脉僵硬度增高,可能与促进胰岛素抵抗等机制有关。     

高血压患者脉压、颈动脉内膜中层厚度和颈股动脉脉搏波传导速度的关系

目的探讨高血压患者脉压、颈动脉内膜中层厚度(CIMT)与颈股动脉脉搏波传导速度(cfPWV)的关系。方法选择2016年1月至2017年6月期间就诊于福建医科大学附属第一医院全科医学和老年科门诊、住院部的原发性高血压患者469例,正常血压者274人。按2×2设计方法,将所有对象分为高血压组及正常血压组,然后以cfPWV 10 m/s为切点值,分别各自分为cfPWV增高组(cfPWV≥10 m/s)和cfPWV正常组(cfPWV<10 m/s)。再次,以CIMT 1.0 mm为切点,分别各自分为CIMT正常组及CIMT增厚组。最后,以年龄65岁为切点,分别各自分为中青年组(<65岁)及老年组(≥65岁)进行分析。测量所有研究对象的血压并计算脉压。应用Pearson相关分析和多元线性回归分析cfPWV的影响因素。结果与正常血压组比较,高血压患者的cfPWV[(9.56±1.93)比(8.46±1.47)m/s]、脉压[(58.6±13.5)比(49.2±10.3)mm Hg]、CIMT[(0.93±0.18)比(0.82±0.17) mm]升高(均P<0.05)。在高血压人群中,cfPWV增高组的脉压[(66.8±14.1)比(54.1±10.7)mm Hg]、CIMT[(0.98±0.16)比(0.90±0.18)mm]高于cfPWV正常组(均P<0.05);老年组的cfPWV[(10.52±2.11)比(9.00±1.55)m/s]、脉压[(66.1±13.7)比(54.1±11.1)mm Hg]、CIMT[(1.02±0.15)比(0.88±0.17)mm]高于中青年组(均P<0.05)。多元线性回归逐步分析结果显示,脉压(β=0.346)、年龄(β=0.345)、心率(β=0.241)、性别(β=-0.142)、空腹血糖(β=0.096)是所有对象cfPWV的相关因素(均P<0.05);分层分析结果显示,无论哪个年龄段及性别,脉压均是cfPWV的相关因素;而CIMT只在中青年人群中是cfPWV的相关因素。结论脉压是高血压患者cfPWV的相关因素,CIMT只是青中年高血压患者cfPWV的相关因素。     

老年原发性高血压患者血压晨峰与左心室肥厚的关系

目的探讨老年原发性高血压患者血压晨峰与左心室肥厚的关系。方法选择老年原发性高血压患者80例,根据24 h动态血压监测分为2组:血压晨峰值≥55 mm Hg(1 mm Hg=0.133 kPa)为晨峰组,血压晨峰值<55mm Hg为非晨峰组,每组40例,均常规行超声心动图检查,计算左心室重量指数(LVMI)。结果晨峰组24h、昼间、夜间收缩压及血压晨峰均明显高于非晨峰组(P<0.05),晨峰组LVMI明显高于非晨峰组;左心室肥厚比例明显高于非晨峰组(P<0.05)。结论老年原发性高血压患者血压晨峰与左心室肥厚密切相关。     

老年男性原发性高血压患者动态血压及血压变异性与踝臂指数的关系探讨

目的评价老年男性原发性高血压患者动态血压及血压变异性(BPV)与踝臂指数(ABI)的关系。方法入选老年男性原发性高血压患者160例,按照ABI分为正常ABI组(ABI>0.90)104例和低ABI组(ABI≤0.90)56例,比较并分析其24 h动态血压参数和BPV参数。结果低ABI组较正常ABI组24 h平均脉压[(62.4±13.8)mm Hg比(53.0±13.0)mm Hg]、日间平均脉压[(67.3±17.0)mm Hg比(55.4±20.0)mm Hg]和夜间平均脉压[(63.0±16.0)mm Hg比(52.9±13.6)mm Hg]均高(P<0.01),同时夜间收缩压最大值[(146.5±17.4)mm Hg比(135.5±17.1)mm Hg]、夜间收缩压标准差[(12.4±4.0)mm Hg比(10.1±4.2)mm Hg]均大(P<0.05)。结论老年男性原发性高血压患者夜间收缩压最大值、夜间收缩压标准差、日间平均脉压、夜间平均脉压和24 h平均脉压升高可能是低ABI的危险因素。     

原发性高血压患者血尿酸水平与左心室肥厚的相关性

目的:探究原发性高血压患者血尿酸水平与左心室肥厚的相关性。方法:收集2012年6月至2013年12月,在安贞医院高血压科诊治的原发性高血压患者581例为研究对象,并行超声心动图测定心脏各腔室内径,计算左心室质量指数(LVMI),根据左心室质量指数(LVMI)≥125g/m~2(男),LVMI≥110g/m~2(女)分为高血压左心室肥厚组和非肥厚组(对照组),分析两组患者基本临床资料,再采用多因素Logistics回归分析的方法,进行UA与LVMI的相关性分析。结果:1.肥厚组与对照组比较,肥厚组尿酸[(453.72±120.63)vs.(349.23±87.39)μmol/L,P=0.00],收缩压[(156.02±22.34)vs.(148.19±22.06)mm Hg,P=0.00)]、(1mm Hg=0.133k Pa)脉压[(52.86±14.08)vs.(47.20±15.52)mm Hg,P=0.00]、LVMI[133.51(124.79,146.26),P=0.00]均高于对照组,差异有统计学意义(P0.05);2两组不同性别的高血压患者的血尿酸水平比较:在肥厚组中,男性血尿酸水平高于女性(t=2.73,P=0.01),在对照组中,男性血尿酸水平也高于女性(t=4.57,P=0.00),差异均有统计学意义(P0.05)。3影响左心室肥厚的多因素Logistic回归分析显示,进一步校正了年龄、性别、高血压病程等心血管危险因素,结果显示血尿酸仍是高血压患者左心室肥厚的独立危险因素(OR=1.03,P=0.00),性别(OR=2.51,P=0.00)和脉压(OR=1.02,P=0.03)也与左心室肥厚密切相关(P0.05)。结论:尿酸与高血压左心室肥厚存在相关性,随着高血压患者的尿酸水平增加,其左心室肥厚显著增加。     

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。     

原发性高血压患者脉压对左心室肥厚、QT离散度的影响

目的　研究脉压对原发性高血压患者左心室肥厚 ,QT离散度的影响。方法　入选 60岁以上 369例高血压患者 ,脉压均大于60 mm Hg以上进行分析 ,按平均压 <118mm Hg和≥ 118mm Hg分为二组 ,再以脉压 60～ 80 mm Hg,81～ 10 0 m m Hg,>10 0 mm Hg分为 3个亚组。结果　 ( 1)随着脉压增加 ,心肌肥厚 ,QT离散度 ,逐渐增加 P<0 .0 1。 ( 2 )脉压相同而平均压分别 <118mm Hg与≥118m m Hg两组进行比较 ,心肌肥厚 ,QT离散度 ,无明显差异 ,而平均压≥ 118mm Hg组的收缩压 ,舒张压 ,平均压均高于平均压 <118m m Hg组 ,两组差异有显著性 P<0 .0 1。结论　高血压患者脉压与左心室肥厚 ,QT离散度 ,相关性较收缩压 ,舒张压更密切     

组织多普勒成像评价血压昼夜节律变异对左心室舒张功能的影响

目的探讨血压昼夜节律变异对左心室舒张功能的影响。方法31例非杓型高血压患者(非杓型组)和31例年龄、性别相匹配的杓型高血压患者(杓型组)入选。两组患者均行24 h动态血压监测和组织多普勒成像(DTI)检查。结果两组日间平均收缩压和平均舒张压无显著性差异,非杓型组的夜间平均收缩压和平均舒张压均显著高于杓型组[(145.1±34.5)mm Hg(1 mm Hg=0.133 kPa)vs(127.9±18.1)mm Hg,(94.2±38.1)mm Hgvs(78.5±18.2)mm Hg,P<0.05]。心脏超声检查显示两组在心腔内径、室壁厚度和左心室射血分数等参数无显著性差异,DTI结果显示非杓型组的平均组织舒张早期速度(MEa)、MEa/平均组织舒张晚期速度(MAa)显著低于杓型组[(5.9±2.1)cm/svs(7.8±3.1)cm/s,(0.68±0.56)cm/svs(0.95±0.39)cm/s,P<0.05和P<0.01)];非杓型组的MAa较杓型组明显升高[(9.5±2.8)cm/svs(8.6±1.7)cm/s,P<0.01]。结论血压昼夜节律变异可加重左心室舒张功能受损。对于存在血压昼夜节律变异的高血压患者应尽早诊断,积极治疗和加强随访。     

组织多普勒Tei指数评价高血压患者左心室功能的临床意义

目的 探讨组织多普勒成像-Tei指数评价原发性高血压患者左心室功能的临床应用价值.方法 采用彩色多普勒超声诊断仪测量计算65例原发性高血压患者及40例正常对照者的左心室质量指数(left ventricular mass index,LVMI),并且在组织多普勒成像模式下,于心尖四腔切面记录二尖瓣环的运动频谱,计算组织多普勒成像-Tei指数.结果 依据左心室肥厚的诊断标准,将入选的原发性高血压患者中34例LVMI符合左心室肥厚诊断标准者设为左心室肥厚组;31例LVMI不符合左心室肥厚诊断标准者设为左心室非肥厚组.左心室肥厚组LVMI大于左心室非肥厚组和正常对照组,差异有统计学意义[(159.52±32.71)g/m2 vs.(103.52±15.41)g/m2,P<0.05;(159.52±32.71)g/m2 vs. (101.25±16.74)g/m2,P<0.05].左心室肥厚组和左心室非肥厚组的组织多普勒成像-Tei指数均高于正常对照组(0.67±0.15 vs. 0.36±0.19,P<0.05;0.58±0.22 vs.0.36±0.19,P<0.05),差异有统计学意义,且左心室肥厚组组织多普勒-Tei指数高于左心室非肥厚组,差异有统计学意义(0.67±0.15 vs. 0.58±0.22,P<0.05).结论 组织多普勒成像-Tei指数是一项新的评价心脏功能的指标,对评价原发性高血压患者的左心室功能有临床意义.     

短时运动对冠状动脉介入治疗术后冠心病患者肱动脉踝动脉脉搏波速度的影响

目的探讨短时运动对PCI术后冠心病患者肱动脉-踝动脉脉搏波速度(brachial-ankle artery pulse wave velocity.baPWV)的影响。方法选择PCI术后常规复查的男性冠心病患者69例,平板运动试验采用改良Bruce方案,试验前及试验结束后10 min测量患者baPWV值。结果患者短时运动后平均动脉压和baPWV值较运动前明显下降[(97.26±11.51)mm Hg vs(91.33±9.64)mm Hg(1 mm Hg=0.1 33 kPa),(1421.84±224.1 4)cm/svs(1 3 4i0.25±218.16)cm/s],差异有统计学意义(P<0.01);收缩压和舒张压较运动前有所下降,但差异无统计学意义(P>0.05)。结论短时运动可以有效改善冠心病患者的动脉僵硬度。     

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。     

原发性高血压左心室肥厚与24小时平均脉压相关性的探讨

目的探讨原发性高血压(EH)左心室肥厚(LVH)与24h平均脉压(PP)和大动脉内径变化的关系。方法应用24h动态血压监测和超声心动图检查,测量并计算80例EH患者24h平均PP,左心室重量指数及主动脉根部内径。分LVH组和无LVH组,分别进行统计学比较。结果24h平均PP和主动脉根部内径在EH有LVH组和无LVH组之间均有显著性差异(P<0.01),左心室重量指数与PP(r=0.3,P<0.01)和主动脉根部内径(r=0.5,P<0.01)之间存在一定的正相关。结论24h平均PP和大动脉内径增大,提示大动脉顺应性下降,在EH发生LVH中起重要作用。     

高血压左心室肥厚与脉压关系的临床观察

目的　探讨高血压病 (essentialhypertension ,EH)左心室肥厚 (leftventricularhypertrophy ,LVH)与脉压 (pulsepressure,PP)和大动脉内径变化的关系。方法　应用诊所血压测量和超声心动图检查 ,测量并计算 92例高血压患者脉压 ,左室重量指数及大动脉内径。分左室肥厚组和无左室肥厚组 ,分别进行统计学比较。结果　脉压和主动脉根部内径在高血压左室肥厚组和无左室肥厚组之间均有显著性差异 (P <0 0 1) ,左室重量指数与脉压 (r =0 3,P <0 0 1)和主动脉根部内径 (r =0 5 ,P <0 0 1)之间存在一定的正相关。结论　脉压和大动脉内径增大 ,提示大动脉顺应性下降 ,在高血压左室肥厚中起重要作用     

高龄高血压患者动态脉压和血脂与左心室肥厚的关系

目的探讨高龄高血压患者动态脉压(APP)和血脂与左心室肥厚(LVH)的相关性。方法入选年龄≥80岁的高血压患者110例,进行24 h动态血压监测、超声心动图检查及血脂检测。根据APP分为高脉压组(≥60mm Hg,1 mm Hg=0.133 kPa)74例和低脉压组(<60 mm Hg)36例,以左心室重量指数(LVMI)作为LVH的诊断标准,又分为LVH组50例和非LVH组60例。并进行相关分析和logistic回归分析。结果与低脉压组比较,高脉压组LVMI、LVH的发生率及各收缩压参数明显升高(P<0.05)。LVH组24 h收缩压、昼间收缩压、APP、脉压指数明显高于非LVH组(P<0.05),2组舒张压差异无统计学意义(P>0.05)。LVMI与APP、脉压指数、24 h收缩压、昼间收缩压、夜间收缩压呈正相关,与HDL-C呈负相关(P<0.05),与所有舒张压参数均无相关性(P>0.05)。APP是LVH的独立危险因素(OR=1.057,95%CI:1.018～1.096,P=0.003)。结论在高龄高血压患者中,APP与LVMI密切相关,是LVH的独立危险因素;HDL-C与LVMI密切相关。     

动态脉压对老年高血压病患者左心室肥厚及主动脉根部扩张的影响

目的研究老年高血压病患者动态脉压(24 h PP)与左心室肥厚(LVH)及主动脉根部(AOD)扩张的相关关系。方法对60例老年高血压病患者进行动态血压(ABP)和超声心动图等检查,分别测量ABP和超声心动图的各种参数。将24 h PP≥60 mm Hg(1 mm Hg=0.133 kPa)的患者30例作为A组,24 h PP<60 mm Hg的患者30例作为B组。结果A、B两组LVH和AOD扩张的发生率差异有显著性意义(P<0.01)。左心室重量指数与24 h PP2、4 h平均收缩压(24 h SBP)密切相关(P<0.01),与脉压和收缩压呈正相关(P<0.05)。AOD与24 h PP、24 h SBP、年龄和病程密切相关(P<0.01)。结论老年高血压病患者的24 h PP与LVH及AOD扩张密切相关,24 h PP可作为评价抗高血压药物能否更好地减少高血压病患者靶器官损害的重要指标之一。     

血管紧张素Ⅱ水平与原发性高血压左心室肥厚的相关性研究

目的:探讨原发性高血压患者血管紧张素Ⅱ(AngⅡ)与左心室肥厚(LVH)的相关性。方法:对2009年4月至2010年12月,高血压科住院行超声心动图(UCG)检查及其他临床资料完整的581例患者,进行回顾性分析;并通过二维引导的M-模式进行测量记录左心室结构,左心室质量指数(LV-MI),将高血压患者分为高血压伴LVH组(LVH组,n=100)和高血压不伴LVH组(NLVH组,n=481),分析AngⅡ与LVH间的相关性。结果:LVH组体质量指数、收缩压、脉压、肌酐(Scr)、肾素及AngⅡ均高于NLVH组(P<0.001)。以LVH为因变量,以收缩压、脉压、Scr及AngⅡ为自变量进行logistic回归分析,显示收缩压、脉压、Scr及AngⅡ与LVH相关,差异有统计学意义(P<0.05)。结论:收缩压、脉压、Scr及AngⅡ在原发性高血压患者左心室肥厚的发生发展过程中起重要作用。     

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。     

Relationship between left ventricular mass index and 24-h urinary free cortisol and cortisone in essential arterial hypertension

OBJECTIVE: Besides arterial blood pressure, nonhemodynamic factors are known to induce cardiac hypertrophy. In Cushing's syndrome, severe ventricular hypertrophy has been linked not only to increased aortic pressure, but also to elevated plasma cortisol. The aim of this study was to examine the relationship between the cortisol/cortisone levels and left ventricular mass index (LVMI) in essential arterial hypertension with and without echocardiographic left ventricular hypertrophy (LVH). DESIGN: Eighteen untreated Caucasian patients (nine men, nine women, mean age 48+/-6 years) with essential hypertension (163+/-26/100+/-14 mm Hg) were enrolled. An age-matched control group of 13 subjects (seven men, six women) with normotension (121+/-9/79+/-7 mm Hg) were enrolled also. Left ventricular dimensions were echocardiographically assessed and cortisol production evaluated by 24-h urinary free cortisol and cortisone concentrations. RESULTS: LVMI averaged 115+/-31 g/m2 and 24-h urinary free cortisol and cortisone were 23+/-14 microg per 24 h and 31+/-18 microg per 24 h. Prevalence of echocardiographic LVH was 56%. LVMI correlated significantly with 24-h urinary free cortisol (r = 0.61, P = 0.007) and cortisone (r = 0.60, P = 0.009). Patients with echocardiographic LVH were characterized by higher daytime ambulatory blood pressure, LVMI (particularly the posterior wall), and 24-h urinary cortisol, while office blood pressure, septal: posterior wall ratio and 24-h urinary cortisone were comparable in all patients. In control individuals, LVMI averaged 91+/-18 g/m2 and 24-h urinary free cortisol and cortisone, respectively, were 34.7+/-6.6 microg per 24 h and 64.3+/-10.8 microg per 24 h (P<0.05 versus patients). Neither LVMI nor the contributing ventricular dimensions showed significant correlation with 24-h urinary free cortisol or cortisone in the control group. CONCLUSIONS: Our data provide evidence for a significant relationship between LVMI and cortisol production independently of arterial blood pressure in untreated mild to moderate hypertension.     

Left ventricular hypertrophy is associated with arterial stiffness and vascular calcification in hemodialysis patients.

Left ventricular hypertrophy (LVH) is the most frequent cardiac abnormality in patients with end-stage renal disease (ESRD). Recent studies have shown that arterial stiffness is associated with mediacalcinosis in these patients. However, whether arterial stiffness and vascular calcification are associated with the LVH in patients with ESRD has not been well established. Forty-nine patients on chronic hemodialysis participated in this study. 1) To better understand the mechanism underlying the increased incidence of LVH, we studied the relation between LVH and each of arterial wall stiffness, aortic calcification, and numerous clinical parameters in 49 patients on chronic hemodialysis. 2) To evaluate the contribution of arterial stiffness and arterial calcification to LVH in hemodialysis patients, we performed the present clinical analysis on 49 patients on chronic hemodialysis. We used an automatic device to measure arterial pulse wave velocity (PWV) as an index of arterial wall stiffness. The aortic calcification index (ACI) was quantified morphometrically by CT scan. The left ventricular mass index (LVMI) was estimated by M-mode echocardiography. To understand the mechanism underlying the increased incidence of LVH, we examined the factors contributing to LVMI in these patients. The correlation between each of the study parameters and LVMI as an indicator of LVH was then examined. The LVMI value was correlated positively with PWV (r=0.439, p=0.0014), systolic blood pressure (r=0.421, p=0.0023), and ACI (r=0.467, p=0.0006). A stepwise linear regression analysis showed that PWV, systolic blood pressure, and ACI were independently associated with LVH in our subjects. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients, with vascular calcification being the most important contributor to the development of LVH. Alteration of pulsatile dynamics contributes to an increase in left ventricular load and thus is also related to the LVH in these patients. These results suggest that LVH is associated with hypertension, increased arterial stiffness, and the extent of vascular calcification in hemodialysis patients. Vascular calcification, which alters the pulsatile dynamics and thereby contributes to an increase in left ventricular load, is the most important contributor to the development of LVH in patients undergoing hemodialysis.     

Impaired responsiveness of the ventricular sensory receptor in hypertensive patients with left ventricular hypertrophy

We studied the control of forearm vascular resistance (FVR) by cardiopulmonary receptors in seven patients with hypertension and left ventricular hypertrophy (LVH) and in seven normotensive control subjects. Increasing levels of lower body negative pressure (LBNP) (-10 and -40 mm Hg) induced a progressive decrease in central venous pressure (CVP) and an increase in FVR. The changes in these two variables were correlated both in normal subjects and patients with hypertension (slope for normal subjects = -29.9, for patients with hypertension = -40.3, NS). After propranolol, there was a significant reduction in the increase in FVR induced by -40 mm Hg LBNP in normal subjects (+107 +/- 5 vs +129 +/- 15 mm Hg/ml/sec, p less than .05) but not in patients with hypertension. Consequently, the slope of the delta CVP/delta FVR regression was reduced in normal subjects (-20.6, p less than .01) but not in patients with hypertension. In another seven normal subjects and seven patients with hypertension and LVH we assessed the effects of -10 and -40 mm Hg LBNP on left ventricular filling pressure (LVFP). LBNP induced similar changes in CVP, LVFP, and total peripheral resistance both in normal subjects and in patients with hypertension. Propranolol failed to modify the effects of LBNP on CVP and LVFP in both groups and reduced the response of total peripheral resistance to -40 mm Hg LBNP only in normal subjects. Propranolol did not reduce the response of FVR to the cold pressor test and sustained handgrip or the arterial baroreflex response to the injection of phenylephrine and increased neck tissue pressure. Thus, hypertension-induced LVH seems to be associated with a selective impairment of the left ventricular sensory receptors.