老年高血压患者静息心率与动态血压参数和左心室肥厚的关系

目的探讨老年高血压患者静息心率(RHR)与动态血压参数和左心室肥厚的关系。方法入选老年高血压患者103例,按RHR水平分为RHR 1组32例:RHR<70/min,RHR 2组38例:70/min≤RHR<80/min,RHR 3组33例:RHR≥80/min。入选患者均行静息心电图、动态血压等检查,并进行比较。结果 RHR 3组的24h、昼间、夜间平均收缩压及脉压明显高于RHR 2和RHR 1组,差异有统计学意义(P<0.05,P<0.01)。RHR与24h收缩压、24h脉压呈正相关(r=0.509,r=0.407,P<0.01),与LVEF呈负相关(r=-0.522,P<0.01)。结论老年高血压患者RHR增快与收缩压、脉压及左心室肥厚密切相关。在控制血压的同时,应注重加强对心率的控制。     

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。     

高血压病患者左室肥厚与心率变异性的临床研究

目的探讨高血压病患者左室肥厚与心率变异性(HRV)的关系及其临床意义。方法应用HRV时域分析法,检测与分析80例高血压病(EH)患者时域分析指标及心率变异指数,并采用超声心动图测定左室重量指数(LVMI)。30名健康者被同期检测,以作对照。结果80例高血压病患者时域分析指标及心率变异指数均比健康人明显降低,合并左室肥厚患者心率变异指数减低的阳性率明显低于同组其他高血压病患者。结论高血压病患者体内自主神经功能失衡,交感与副交感神经的双重损害参与了高血压的左室重构机制,且其损害程度可能伴随左室重构过程而加重。     

老年高血压左心室肥厚患者心肌毛细血管病理改变特点

目的 :了解老年高血压左心室肥厚 (LVH)患者心肌毛细血管病变的特点 ,并在LVH分级相同的条件下 ,观察高血压、冠心病、糖尿病心肌毛细血管病变的区别。方法 :从我院 195 4年～ 1996年间3195例连续尸检标本中选取年龄≥ 6 0岁的高血压病、冠心病、高血压合并冠心病、糖尿病 2 0 6例和对照组 30例共 2 36例心脏标本进行CD31免疫组化染色 ,显示心肌间质 5～ 8μm毛细血管 ,通过光镜和电脑图象分析 ,定量检测心肌毛细血管密度 (capillarydensity ,CD)及其内皮细胞面积 (areaofendothelialcells,AEC) ;根据左室游离壁厚度将LVH分为 0级～Ⅲ级 ;高血压组LVH 0～Ⅲ级 ,冠心病组、高血压合并冠心病组、糖尿病组LVH均为I级。各组间比较采用SAS系统处理。结果 :高血压组随LVH加重 ,CD与AEC逐渐减小 (P <0 0 5 ) ;冠心病组上述变化不明显 (P >0 0 5 )而高血压合并冠心病组有上述改变且程度更重 (P <0 0 1) ;糖尿病组MCD及AEC也明显减少 (P <0 0 5 )。结论 :高血压LVH组毛细血管减少 ,糖尿病组有相似改变而冠心病组变化不明显。高血压和糖尿病的这种微血管病变是导致心血管事件的重要病理基础 ,应引起进一步重视     

老年高血压患者动态脉压与左心室肥厚的关系

目的：探讨动态脉压与老年高血压病左心室肥厚的关系。方法：选择本院疗养员血压相对稳定（不停用原有的降压治疗措施）老年高血压患者155例，进行24小时动态血压监测及超声心动图检查，根据动态血压、脉压以及是否伴有左心室肥厚进行分组及统计学比较。结果：（1）随着脉压的增大，左室重量指数LVMI、24小时平均心率（24hHR）均有显著差异（P均〈0．05）；（2）相同脉压下，不管血压控制如何，LVMI无显著性差异；（3）左室肥厚组的动态脉压、收缩压及24h心率较非肥厚组均有显著差异（P均〈0．05）。结论：动态脉压的增大，是老年高血压患者左心室肥厚的危险因素。     

高血压患者血压和心率昼夜节律变化与左心室肥厚的关系

目的探讨原发性高血压患者血压和心率24h昼夜节律变化与左心室肥厚的关系。方法对初发未治疗高血压患者296例进行动态血压监测分析,根据患者夜间血压和心率均值较白天平均值下降是否超过10%,将患者分为4组:杓型血压和心率组(血压和心率均杓型,n=163)、非杓型血压组(血压非杓型,心率杓型,n=62)、非杓型心率组(血压杓型,心率非杓型,n=42)、非杓型血压和心率组(血压和心率均非杓型,n=29)。对4组间相关临床资料、超声心动图结果进行比较。结果高血压患者收缩压和舒张压非杓型率分别为25%和27%,非杓型心率的比例为24%。非杓型血压和心率组、非杓型血压组、非杓型心率组左心房内径(LAD)、左心室舒张末期内径(LVEDD)、室间隔厚度(IVST)和左心室质量指数(LVMI)明显高于杓型血压和心率组(均P<0.05),其中非杓型血压和心率组上述指标明显高于其他3组(均P<0.05),非杓型血压组、非杓型心率组之间差异无统计学意义。Logistic回归分析显示,年龄、24h平均收缩压、24h平均舒张压、夜间平均收缩压、夜间平均舒张压、非杓型血压、非杓型心率与左心室肥厚的发生密切相关。经调整相关指标后,非杓型血压和非杓型心率使左心室肥厚发生风险分别增加56%和32%。结论高血压患者血压和心率昼夜节律变化与左心室肥厚明显相关。     

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。     

银杏叶片联合氯沙坦对高血压左心室肥厚以及心率震荡的影响

目的观察银杏叶片联合氯沙坦治疗高血压左心室肥厚以及心率震荡指数的影响。方法纳入高血压左心室肥厚患者120例,随机分成3组:对照组40例,给予钙离子拮抗剂、β-受体阻滞剂(倍他乐克)、阿司匹林等常规基础治疗;氯沙坦组40例,在对照组治疗的基础上加用氯沙坦片(50mg,1次/d);联合组40例,在对照组治疗的基础上给予银杏叶片(19.2mg,3次/d)及氯沙坦(50mg,1次/d),均治疗24个月。观察各组患者治疗前后心率震荡指数〔震荡斜率(TS)、震荡初始心率(TO)〕、左心室质量指标(LVMI)、血压及总胆固醇(TC)等变化。结果与对照组比较,治疗后氯沙坦组及联合组TO、LVMI、收缩压、舒张压显著降低,差异均有统计学意义(F=13.67～34.86,q=4.357～11.321,P<0.05),TS升高,差异均有统计学意义(F=126.58,q=9.701～29.124,P<0.05)。与氯沙坦组比较,联合组TO、LVMI降低,差异均有统计学意义(F=24.18～33.73,q=2.948～3.272,P<0.05),TS显著升高,差异均有统计学意义(F=137.68,q=13.710,P<0.05)。心率震荡指数TO、TS与LVMI呈相关性(r=0.529～0.645,P<0.05)。结论银杏叶片联合氯沙坦可以明显改善高血压左心室肥厚、心率震荡以及自主神经功能紊乱。     

原发性高血压左室肥厚患者心率振荡现象及临床意义

目的探讨原发性高血压合并左心室肥厚（LVH）患者心率振荡现象（HRT）及临床意义。方法人选276例原发性高血压患者，均进行心脏彩超检查及24h心电（Holter）记录，计算左心室重量、左心室重量指数（LVMI）、震荡初始（TO）及震荡斜率（偈）。以LVMI男性〉125g／m2．女性〉120g／m。和（或）室间隔厚度（IVST）〉12mm作为左室肥厚（LVH）标准，分为LVH组及左室正常组。结果LVH组TO及TS分别为（1．19±0．84）％及（4．23±0．85）ms／RR，左室正常组分别为（-0．54±0．86）％及（6．81±1．22）ms／RR，两组比较差异有统计学意义，P〈0．01。LVH组异常TO及偈比率与左室正常组比较，差异有统计学意义（P〈0．01）。TO与左室射血分数（LVEF）、左室舒张末期内径（LVEDD）及LVMI显著相关，P〈0．05。TS与LVEF、IVST显著相关，P〈0．05；与LVEDD及LVMI显著相关，P〈0．01。结论原发性高血压伴LVH患者的HRT明显减弱，提示高血压合并LVH时，自主神经功能受损加重。     

老年原发性高血压患者心率与动态血压、左心室肥厚、血脂的相关性

目的 探讨老年原发性高血压(EH)患者静息心率(RHR)与动态血压、左心室肥厚及血脂的关系.方法 对158例EH患者(按RHR水平分三组:RHRⅠ组＜70次/min;70次/min≤RHRⅡ组＜80次/nin; RHRⅢ组≥80次/min)和同期129例正常健康体检老年人(对照组)测定RMR、血脂,并做动态血压及超声心动图检查,进行分组研究.结果 ①EH患者RHR显著高于正常对照组(P＜0.05).②按RHR水平分三组,组间动态血压参数比较:RHRⅢ组的24 h、白昼、夜间平均收缩压及脉压(TSBP、dSBP、nSBP;TPP、dPP、nPP)均高于RHRⅢ、RHRⅠ组,差异有统计学意义(P＜0.05);而24 h、白昼、夜间平均舒张压( TDBP、dDBP、nDBP)的差异无统计学意义(P＞0.05).③三组患者左室后壁厚度(LVPW)、室间隔厚度(IVST)、左室舒张末期内径(LVDD)、左室射血分数(IVEF)和左室心肌重量指数(LVMI)差异有显著性(P＜0.05),且随着RHR增加LVPW、IVST及LVMI增加,而IVEF降低.④三组患者血脂水平比较有显著性差异(P＜0.05),且随RHR增加血清总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白(LDL-C)水平升高,而高密度脂蛋白(HDL-C)水平降低.结论 老年EH患者RHR与SBP、PP、血脂代谢异常及靶器官损害相关.     

老老年高血压病患者左心室肥厚与心律失常及心率变异性的关系研究

目的：研究老老年高血压患者左心室肥厚(LVH)与心律失常及心率变异性(HRV)的关系。方法：纳入2012年10月至2014年7月于中国中医科学院广安门医院心内科住院的303例老老年高血压病患者,根据是否合并左心室肥厚分为2组,检测24小时动态心电图心率变异性时域分析及超声心动图,观察2组之间相关指标的差异。结果：老老年高血压合并LVH组较不合并LVH组房性、室性心律失常检出率增高,差异具有统计学意义(P<0.05),二组PNN50、RMSSD、SDNN、SDANN差异无统计学意义。结论：老老年高血压合并LVH心律失常的发生率明显增高,而二者心率变异性无明显差异。     

Effects of heart rate on coronary circulation and external mechanical efficiency in elderly hypertensive patients with left ventricular hypertrophy

Background and hypothesis: Mechanisms of heart failure in elderly hypertensive patients with hypertrophy have not been studied sufficiently. We hypothesized that impaired increment of coronary blood flow in response to increases in heart rate could be responsible for the occurrence or aggravation of heart failure. Methods: To test this hypothesis, we measured coronary hemodynamics and lactate balance during basal conditions and atrial pacing in 21 elderly patients aged ≥ 65 years (mean 74 ± 6 years) without coronary arterial disease: 7 normoten-sive control patients (Group 1), 7 hypertensive hypertrophic patients without a history of congestive heart failure (Group 2), and 7 patients with such history (Group 3). Coronary sinus blood flow (CSBF) was measured in coronary sinus using a thermodilution catheter. Results: During basal conditions, heart rate did not differ among the three groups (67 ± 3 in Group 1,65 ±11 in Group 2, and 63 ± 6 beats/min in Group 3). CSBF was significantly higher in the two hypertrophic groups than in the control group, but CSBF normalized by left ventricular mass was significantly lower in both hypertrophic groups. External mechanical efficiency (EME) obtained as left ventricular work divided by myocardial oxygen consumption did not differ among groups during basal conditions (36 ± 9% in Group 1, 35 ± 8% in Group 2, and 29 ± 9% in Group 3, NS). During atrial pacing to increase heart rate by 25 ± 5% (lower) and 54 ± 6% (higher), the increases in CSBF were markedly limited in both hypertrophic groups, and the response in Group 3 was more depressed than that in Group 2. EME did not change in the control group or in Group 2, but did decrease to 21 ± 5% in Group 3 during the higher pacing rate (p <0.01 vs. basal conditions). in this group, the relationship between EME and heart rate showed a significant negative correlation (r = —0.56, p = 0.02). Lactate balance in coronary sinus blood showed a tendency to production in Group 3 during the higher pacing rate, suggesting myocardial ischemia. Conclusion: These findings suggest that in hypertensive hypertrophic patients with a history of heart failure, the coronary circulation system is vulnerable to increasing heart rate. in medical treatment of elderly hypertensive patients, control of heart rate in addition to blood pressure control should be considered to minimize the occurrence or aggravation of heart failure.     

Regression of left ventricular hypertrophy in hypertensive elderly patients with carvedilol

In hypertensive patients, the development of left ventricular hypertrophy seems to increase the risk of cardiovascular death although some antihypertensive agents have been associated with regression in left ventricular hypertrophy. A few studies have evaluated the carvedilol, a new drug having a balanced pharmacology of vasodilatation and beta-receptor blockade, particularly in elderly hypertensive patients. To test its effects on left ventricular hypertrophy, patients with essential hypertension and left ventricular hypertrophy were studied before and at the end of 6 months of therapy with 25 mg of carvedilol daily. Candidates had to have moderate, uncontrolled essential hypertension with echocardiographically documented left ventricular hypertrophy (left ventricular mass index > 130 g/m2 for men and > 110 g/m2 for women). Of 26 patients selected, 4 dropped out. The remaining 22 patients successfully completed 6 months of therapy. The average age was 69 +/- 8 years. Carvedilol caused a significant reduction of mean systolic blood pressure from 175 to 145 mmHg (p < 0.001), of diastolic blood pressure from 102 to 82 mmHg (p < 0.001), of left ventricular mass index from 148 +/- 24 g/m2 (p < 0.003), and a non significant change of the mean heart rate from 78 to 72 beats/min. In our study, carvedilol was well tolerated in patients with essential hypertension and left ventricular hypertrophy.     

老老年高血压患者左心室肥厚与心律失常及心率变异性的关系研究

目的 探讨老老年高血压患者左心室肥厚(LVH)与心律失常及心率变异性(HRV)的关系.方法 纳入2012年10月至2014年7月于中国中医科学院广安门医院心内科住院的303例老老年高血压患者,根据是否合并左心室肥厚分为2组,检测24 h动态心电图心率变异性时域分析及超声心动图,观察两组间相关指标的差异.结果 老老年高血压合并LVH组较不合并LVH组房性、室性心律失常检出率增高,差异具有统计学意义(P＜0.05),两组PNN50、RMSSD、SDNN、SDANN的P值分别为0.573、0.198、0.110、0.812,未见统计学差异.结论 老老年高血压合并LVH患者心律失常的发生率明显增高,而老老年高血压合并LVH和不合并LVH患者心率变异性无明显差异.     

Candesartan cilexetil improves left ventricular function, left ventricular hypertrophy, and endothelial function in patients with hypertensive heart disease.

Patients with hypertension often develop left ventricular (LV) hypertrophy and deterioration of the cardiac and endothelial functions. Recent clinical trials have shown the added benefits of angiotensin II receptor blockers in hypertensive patients. Twenty-nine patients with hypertensive heart disease (HHD) underwent echocardiography, radionuclide ventriculography and the measurement of endothelial function before and after administration of candesartan (8 mg/day). The subjects were divided into poorly controlled blood pressure (BP) (group P, n=6) and well controlled BP (group C, n=23). Endothelial function was evaluated from flow-dependent dilation, which was calculated as the percent change of the radial artery diameter during reactive hyperemia after upper arm occlusion, measured with a high-resolution ultrasound system. In group C, LV diastolic function and endothelial function were significantly (p<0.05) improved at 3 months after administration, LV systolic function and hypertrophy were significantly (p<0.05) improved after 6 months and these effects were maintained at 12 months. Even in group P, LV function, LV hypertrophy, endothelial function and brain natriuretic peptide were significantly (p<0.05) improved at 6 months after administration. In patients with HHD, candesartan improves LV systolic and diastolic function, LV hypertrophy and endothelial function within 6 months of administration, regardless of the control of BP.     

老年原发性高血压左心室肥厚患者心肾微动脉的病理特征

目的 研究老年原发性高血压左心室肥厚(LVH)患者心、肾微动脉改变的病理特点,以发现两个靶器官微动脉结构变化的异同和相互联系.方法 从解放军总医院1954-2004年连续尸检的病例中,选取年龄≥60岁经临床和尸检证实为原发性高血压LVH患者25例和对照组8例的心、肾标本为研究对象,其中原发性高血压组再按LVH程度(Ⅰ～Ⅲ级)分为三组,予HE、Masson染色后,用光镜配合电脑图像分析,定量检测心、肾微动脉几何形态学参数,并用半定量的方法 评估微动脉的损伤指数和血浆蛋白浸润指数.结果 高血压组心、肾微动脉血管几何形态学参数随LVH程度的增加呈现出有规律的变化趋势,表现为血管内径(ID)、管腔横截面积(LCSA)减小,而血管壁厚度(WT)、血管壁横截面积(WCSA)、壁腔横截面积比值(WCSA/LCSA)和壁厚内径比值(WT/ID)增大;不同外径(OD)范围的心肌、肾脏微动脉WCSA/LCSA和WT/ID比较均发现,随OD的增加,血管的WCSA/LCSA和WT/ID比值减小;相同OD范围的心、肾微动脉各项血管几何形态学参数比较有明显差异(P＜0.05);高血压组心、肾微动脉血浆蛋白浸润指数、血管损伤指数高于对照组(P＜0.01);各组肾脏微动脉血管损伤指数、血浆蛋白浸润指数均高于心肌微动脉(P＜0.01).结论 原发性高血压患者心、肾微动脉均出现向心性重构,在血管OD范围为10～50 μm的微动脉表现最明显,OD＜50μm的微动脉最易出现闭塞;心、肾微动脉血管重构随高血压LVH程度的增加而加重;高血压肾脏微动脉损伤比心肌微动脉重.微动脉病变是高血压靶器官损害的重要病理学基础.     

老年高血压左室肥大QT离散度改变及与心率变异关系

目的　探讨老年高血压左室肥大QT离散度的改变 ,及与心率变异的关系。　 方法　对 85例老年高血压患者进行动态血压、心脏超声、QT离散度及心率变异的分析 ,并对左室肥大指数与QT离散度、血压与心率变异作相关分析。　 结果　高血压伴左室肥大者QT离散度增加 [QTcd :(5 0 98± 18 79)ms ,QTacd :(5 1 2 1± 13 42 )ms ,QTsD :(15 47± 7 0 8)ms ,QTaSD :(15 48± 4 6 5 )ms] ;左室肌重与非左室肥大相比 ,心率变异无明显差别 (P >0 0 5 ) ;左室肥大指数 (LVMI)与QT离散度 (QTcd、QTacd、QTsD、QTaSD)呈正相关 ,血压 (SBP、DBP)与心率变异 (MSSD、HF、LF、TF)呈负相关。　 结论 　高血压左室肥大者心肌局部复极化不一致 ,高血压患者心率变异下降 ,但与左室结构改变关系不大     

Clinicopathological study on left ventricular hypertrophy in elderly hypertensive patients

The correlations between blood pressure, left ventricular hypertrophy and left atrial enlargement were examined in 2,010 autopsied cases. The cases were classified into 3 groups: 972 (48.2%) normotension cases, 313 cases (15.5%) of systolic hypertension and 725 cases (36.1%) of diastolic hypertension. The incidence of left ventricular hypertrophy (LVH) was significantly higher in systolic and diastolic hypertensive cases than in normotensives (p less than 0.05), but no significant difference in LVH incidence was found between the 2 hypertensive groups. The incidence of an enlarged left atrium was also significantly higher in both hypertensive groups than in the normotensive group (p less than 0.05). The incidence of congestive heart failure and a large CTR were also higher in both hypertensive groups. However, there were no intergroup differences in atrial fibrillation incidence, despite significant differences in atrial size. Finally, the incidence of moderate to severe coronary artery stenosis was significantly higher in both hypertensive groups, but no difference was found between the 2 types of hypertension. We concluded that both systolic and diastolic hypertension contributed to the genesis of left ventricular hypertrophy, left atrial dilatation, coronary sclerosis and congestive heart failure.     

Echocardiographic assessment of left ventricular hypertrophy and function in renal hypertensive dogs

To investigate the performance of the hypertrophied left ventricle, M-mode echocardiographic measurements were performed 2 to 3 times weekly on 8 unanesthetized dogs for several weeks before and for 6 months after the induction of perinephritic hypertension. Four dogs with sham-wrapping and contralateral nephrectomy served as the controls. From a baseline value of 7.7 +/- 0.4 mm (mean +/- SD), left ventricular wall thickness increased to 9.0 +/- 0.6 mm (p less than 0.001) by the 4th week after the induction of hypertension and reached a plateau of 10.2 +/- 1.2 mm (p less than 0.001) by week 10. Fractional shortening of left ventricular dimension (% delta D) increased during early left ventricular hypertrophy and remained elevated for 6 months in the surviving 6 hypertensive dogs. In hypertensive dogs, left ventricular concentric hypertrophy became detectable by week 6 of hypertension. Control dogs did not show these changes. At autopsy, the left ventricular weight of hypertensive and normotensive control dogs was (6.2 +/- 1.4 g/kg and 4.3 +/- 0.5 g/kg (p less than 0.05). In summary, during the early stage of left ventricular hypertrophy in renal hypertensive dogs cardiac performance increased. There is no evidence for deterioration of left ventricular performance as concentric left ventricular hypertrophy develops and becomes chronic.