高血压病左室肥厚与平均血压、血压负荷及血压变异性的关系

目的：探讨原发性高血压病左室肥厚（LVH）与平均血压、血压负荷及血压变异性的关系。方法：运用无创性动态血压监测仪对56例原发性高血压患者（EH）进行24小时监测,并进行左室重量测定,根据左室重量指数将其分为左室肥厚组30例和无左室肥厚组26例,比较其血压变异性参数、平均血压及血压负荷,并进行左室重量指数（LVMI）与上述各参数的相关分析。结果：左室肥厚组血压变异性、24小时及昼夜血压负荷、平均血压均较无左室肥厚组明显增大和升高。24小时及昼夜平均收缩压与舒张压（24SP、24DP、DSP、DDP、NSP、NDP）、24小时及夜间收缩压与舒张压负荷、白昼收缩压负荷（24SPL、24DPL、DSPL、DDPL、NSPL、NDPL）、收缩压变异性与舒张压变异性（SPv、DPv）与LVMI呈正相关。结论：EH者左室肥厚是平均血压水平升高,血压负荷增大和血压变异性增加等因素共同作用的结果,尤以夜间血压升高和血压负荷增大对其影响较大。     

老年收缩期高血压合并左心室肥厚的危险因素分析

目的探讨药物规律治疗下老年收缩期高血压（systolic Hypertension of Elderly Patients，SHE）左室肥厚（Left Ventriculjar Hypertrophy．LVH）的特点及其危险固素。方法采用队列分析法，以左室重量指数（Left Ventricular Mass Index，LVMI）将115例老年高血压患者分为左室肥厚组69例和非左室肥厚组46例，两组间各项相关临床数据进行比较（t检验和x^2检验），对与LVMI可能相关的因素进行单相关分析及Logistic回归分析。结果老年收缩期高血压患者LVH占60％。左室肥厚组与非左室肥厚组的脑卒中（stroke）构成比有显著性差异（P〈0．05）：组间动态血压参数中，非构型血压节律构成比、24hSBP、dSBP、24hPP相较差异有统计学意义（P〈0．05）：nSBP、nPP差异有显著意义（P〈0．01）：生化指标中UA在左室肥厚组明显升高，差异有显著性（P〈0．05）；左室重量指数与24hSBP、dSBP、nSBP、UA呈正相关（P〈0．05），与24hPP呈显著正相关（r=0．206，P〈0．01），与夜间血压下降百分率呈显著负相关（r=-0．184，P〈0．01）：Logistic回归分析提示，24hPP是SHE患者左室肥厚的独立危险因子，脑卒中与LVH独立相关。结论SHE患者中收缩压高、脉压大、非构型血压节律者LVH发生率高，24hPP是LVH的独立预测固子：脑卒中与LVH独立相关，这种相关关系独立于血压之外；UA与LVMI呈正相关。高UA与LVH发生可能存在确切联系。     

高血压病患者血压波动性与左室肥厚的关系

目的：探讨高血压患血压波动性与左室肥厚的关系。方法：以动态血压监测(ABPM）和超声心动图的方法研究150例高血压病患和30例血压正常的健康的左室重量指数（LVMI)与24 h动态血压平均值(24 hABPa)和24h动态血压波动性(ABPV)的关系。结果：高血压组LVMI显大于正常血压组(P<0.001）。高血压组LVMI与24 h收缩压平均值(24 h ABPs)显相关(r=0.612 P<0.001),与24 h小时舒张压平均值(24 hABPd）显相关(r=0.232 P<0．005),而与ABPV未显示相关性（P>0．5和P>0.2)。结论：高血压病组存在有明显的左室肥厚。高血压病组左室肥厚与24 h血压平均值呈显正相关,与血压波动性无显相关性。     

老年人高血压患者脉压与左室肥厚的临床观察

目的探讨老年高血压患者脉压与左室肥厚的关系。方法选择150例老年高血压患者，均行24h动态血压监测，据平均脉压（ABPP）结果分为≥60mm Hg组和〈60mmHg组，采用多普勒超声心动图测量左室射血分数（LVEF），并计算左室质量（LVM）、相对室壁厚度（RWT）和左室质量指数（LVMI），将两组的临床资料进行分析。结果ABPP≥60mmHg组的LVMI、LVM及RWT的值均高于ABPP〈60mmHg组，LVEF则低于ABPP〈60mmHg组（P〈0．05）。两组发生室性心律失常、心力衰竭、心肌梗死的比例差异有统计学意义（P〈0．01）。结论老年人24h平均脉压增大与左室肥厚呈正相关，易发生室性心律失常、心力衰竭及心肌梗死，有一定的临床意义。     

声学定量技术对高血压患者左室功能的评价

目的：应用声学定量（AQ）技术评价高血压患者的左室收缩和舒张功能。方法：48例高血压患者和20例正常对照进行了AQ检测，根据左室心肌重量指数（LVMI），高血压组又分为高血压LVMI正常组与左室肥厚组。结果：与对照组左室舒张功能指标比较，高血压患者左室充盈异常，舒张早期充盈减低，舒张晚期充盈增强；与高血压LVMI正常组比较，高血压左室肥厚组左室充盈尤其是舒张早期充盈低于高血压LVMI正常组；与对照组左室收缩功能指标比较，高血压LVMI正常组左室收缩功能正常，且处于高血流动力学状态，而高血压左室肥厚组左室收缩功能减低，且低于LVMI正常组；与对照组左室容量指标比较，高血压LVMI正常组左室容量负荷增大，而高血压左室肥厚组无显著差异。结论：AQ技术为定量评价高血压患者的左室收缩和舒张功能提供了新的途径。     

高血压患者血压变异性与左心室肥厚的关系

【目的】探讨原发性高血压患者血压变异性与左心室肥厚的关系。【方法】60例原发性高血压患者分别进行超声心动图和动态血压监测,根据左心室重量指数（LVMI）分为左心室肥厚（LVH）组和无LVH组,分析比较两组间的血压均值和血压变异性。【结果】LVH组24 h平均收缩压（24hSBP）、24 h平均舒张压（24hDBP）及白昼收缩压（dSBP）与夜间收缩压（nSBP）、白昼舒张压（dDBP）均显著高于无LVH组,且差异显著（ P ＜0．05）;LVH组血压变异性各指标除白昼舒张压标准差（dDSD）外,均比无LVH组增大,差异显著（ P ＜0．05）。【结论】原发性高血压患者LVH的发生和血压变异性密切相关,血压变异性增高对左心室肥厚风险有一定预测价值。     

原发性高血压患者血压变异性与左室肥厚的相关性分析

目的 探讨原发性高血压血压变异性与左室肥厚的相关性.方法 60例原发性高血压患者根据有无左室肥厚分为左室肥厚(LVH)组及非LVH组,同时选择30例血压正常患者为对照组,对3组进行动态血压和超声心动图监测.结果 高血压LVH组与非LVH组或健康组动态监测各时间段血压均值及血压变异性比较差异有显著性(P＜0.05),非高血压LVH组与非LVH组或对照组超声心动图检测的左心室质量指标(LVMI)差异有显著性(P＜0.05).血压变异性和左心室肥厚质量指标相关性好.结论 原发性高血压血压变异性与左室肥厚关系密切,血压变异性增大对左室肥厚的风险性预测有较好的参考价值.     

缬沙坦并氢氯噻嗪对老年单纯收缩期高血压左室肥厚的影响

目的观察缬沙坦并氢氯噻嗪对老年单纯收缩期高血压（ISH）的降压作用及对脉压（PP）和左室肥厚（LVH）的影响。方法67例ISH患者给予缬沙坦并氧氯噻嗪口服16周,治疗前及治疗后每2周测蹙血压,治疗前后查超声心动图,测量左室舒张末内径（LVDd）、窄问隔厚度（IVST）及左室后壁厚度（PWT）,计算左室重量指数（LVMI）,观察治疗前后血压、PP、LVMI的变化。结果治疗后收缩压（SBP）、PP显著降低（P〈0．01）,舒张压（DBP）明、显降低（P〈0．05）,左室重量指数（LVMI）鼹著下降（P〈0．01）。结论缬沙坦并氢氯噻嗪能显著降低SBP、PP、LVMI,改善左室重担肥厚。     

伊贝沙坦、缬沙坦和氯沙坦对高血压左室肥厚的影响

目的：比较伊贝沙坦、缬沙坦和氯沙坦对高血压左室肥厚的疗效。方法：选择130例高血压患者，随机分为3组，分别给予伊贝沙坦、缬沙坦和氯沙坦治疗6个月。观察治疗前后舒张末期室间隔厚度（IVST）、舒张末期左室后壁厚度（PWT）、左室重量（LVM）、左室重量指数（LVMI）的变化及24h平均血压的变化。结果：三组治疗前后血压明显下降（P〈0．01），IVST、PWT、LVM和LVMI明显下降（P〈0．01），三组间比较差异无显著性（P〉0．05）。结论：伊贝沙坦、缬沙坦和氯沙坦均可有效的降低血压。并明显改善心富肥厚。     

老年单纯收缩期高血压与靶器官损害的关系

目的 探讨老年单纯收缩期高血压与靶器官损害的关系.方法 选择60岁以上原发性高血压患者120例,其中单纯收缩期高血压患者60例,非单纯收缩期高血压患者60例,2组患者均测定内生肌酐清除率（Ccr）,行超声心动图、颈动脉超声、颅脑CT和（或）MRI检查.比较Ccr、左室重量指数（LVMI ）、左室射血分数（LVEF ）、左室舒张早期充盈峰值流速（E峰）及舒张晚期左房收缩期充盈峰值流速（A峰）比值（E/A）、颈动脉中层厚度（IMT）,脑血管疾病的影像学证据.结果 2组患者左室肥厚、脑损害、肾功能损害及颈动脉斑块的差异均有统计学意义.结论 老年收缩期高血压与靶器官的损害密切相关,是比舒张期高血压更强的致靶器官损害因素.     

老年男性高血压患者降压治疗后血压变异性与心室重构的相关性研究

目的探讨老年男性高血压患者降压治疗后动态血压变异性与心室重构的关系。方法入选老年男性原发性高血压患者212例(高血压组),均单用长效钙通道阻滞剂降压治疗超过1年,行动态血压监测(ABPM),根据24h收缩压平均实际变异性(24 hSBP AVR)的第50百分位数(P50)将高血压组分为两组:高AVR组(AVR≥10.17 mmHg)和低AVR组(AVR<10.17 mmHg),各106例。另入选48例同期年龄相匹配的非高血压老年男性患者为对照组。测定入选患者所有血压水平、24 hSBP AVR等血压变异性指标及舒张期室间隔厚度(IVST)、舒张期左心室后壁厚度(LVPWT)、左心室舒张末内径(LVEDd),计算左心室质量指数(LVMI),比较各组差异。结果与对照组比较,高血压组24 h、日间及夜间平均收缩压,24 hSBP AVR值均高于对照组(P<0.05),高AVR组IVST及IVEDd高于低AVR组(P<0.05)。相关分析显示,LVMI与24 hSBP(r=0.361,P<0.05)及24 hSBP AVR(r=0.210,P<0.05)呈正相关。结论老年男性原发性高血压患者降压治疗后收缩压水平及收缩压变异性与左心室重构有关。     

老年原发性高血压患者动态脉压与左心室质量指数关系的研究

目的探讨老年原发性高血压动态脉压与左心室质量指数（LVMI）的关系。方法收集2012年1月一12月住院的110例老年原发性高血压患者的临床资料。所有患者均已行动态血压检测,并行超声心动图检查,依据24h动态血压结果计算动态脉压,依据超声心动图结果计算LVMI,按照脉压〈60mmHg（1mmHg=0．133kPa）以及≥60mmHg将患者分为A组（n=70）和B组（n=40）,比较两组患者的LVMI等指标,并采用多重线性逐步回归分析动态脉压与LVMI的关系。结果B组患者的24h平均收缩压、动态脉压较A组明显增高（P〈0．001）;B组患者的室间隔厚度、左心室后壁厚度、左心室质量、LVMI均高于A组（P〈0．05）;Pearson相关分析显示：动态脉压与LVMI呈正相关（r=0．33,P〈0．001）;多重线性逐步回归显示：动态脉压是LVMI增加的危险因素（β=0．90,P〈0．001）。结论老年原发性高血压患者动态脉压与LVMI呈正相关,动态脉压是老年原发性高血压患者左心室结构损害的重要危险因素。     

Stress-induced blood pressure measurements predict left ventricular mass over three years among borderline hypertensive men

Exaggerated cardiovascular reactivity has been implicated in the development of left ventricular hypertrophy. The aim of the present study was to investigate the predictive value of casual clinic, 24-h ambulatory blood pressure and stress-induced blood pressure measurements in the laboratory for left ventricular structures over a 3-year period in a group of middle-aged borderline hypertensive men. The stress test included a pretask resting period and two tasks, mental arithmetic and isometric muscle contraction. Left ventricular wall thickness was assessed by M-mode echocardiography. All stress-induced blood pressure levels and reactivity measures as well as ambulatory systolic blood pressure and mean arterial pressure levels were significantly correlated with left ventricular mass index (LVMI) 3 years later ( r  = 0.31–0.50), whereas there were no significant correlations between casual clinic or resting BP measurement and LVMI. A stepwise multiple regression analysis with LVMI at the 3-year follow-up as the dependent variable was applied. Baseline LVMI was entered as a forced variable and explained 24% of the variance in LVMI. Mean arterial blood pressure reactivity in the laboratory was the strongest additional independent variable, and added 15% to the prediction of LVMI 3 years later. Using a median split approach, the borderline hypertensive group was divided into high and low BP reactors. High and low BP reactors did not differ at initial baseline, but at the 3-year follow-up the high reactive group had significantly larger LVMI than the low reactive group. Results from the present study suggest that stress-induced BP reactivity measurements predict the development of LVMI better than casual or resting BP measurements. Thus, measuring BP during standardized stress tests could be a method used to identify borderline hypertensive individuals at increased risk of developing left ventricular hypertrophy.     

高血压患者血压变异性和左室肥厚关系的研究

目的观察原发性高血压患者血压变异性与左心室肥厚的关系。方法原发性高血压患者60例,分别进行超声心动图检查和24 h动态血压监测,根据超声心动图测量指标计算所得的左心室重量指数(LVMI)分为左心室肥厚(LVH)组和无LVH组,分析比较两组间的血压均值和血压变异性。结果 LVH组24 h、白昼、夜间的收缩压和舒张压水平以及各阶段的收缩压和舒张压标准差均比无LVH组明显增大,差异有显著性;且LVH组LVMI高于无LVH组,差异有显著性。结论原发性高血压患者LVH的发生和血压变异性密切相关,血压变异性增高对左心室肥厚风险有一定预测价值。     

厄贝沙坦、硝苯地平及美托洛尔逆转高血压病左心室肥厚的效果观察

目的比较厄贝沙坦、硝苯地平及美托洛尔治疗原发性高血压逆转左心室肥厚的作用。方法选择150例原发性高血压伴左心室肥厚患者,随机分为厄贝沙坦组(A组)、硝苯地平控释片(B组)及美托洛尔组(C组)各50例。全组患者未曾接受降压治疗(或仅用过利尿剂)或已停用降压药物3周以上。A组服用厄贝沙坦150~300 mg,1次/d,B组服用硝苯地平控释片30~60 mg,1次/d,C组服用美托洛尔25~50 mg,2次/d;疗程均为24周。观察治疗前后血压及超声心动图变化。结果各组患者治疗后血压均显著降低(P<0.01),组间降压幅度无明显统计学差异(P>0.05)。各组患者治疗后舒张期左室后壁厚度、舒张期室间隔厚度、左室舒张末期内径及左室重量指数均有显著改善(P<0.05,0.01)。而且A组左室重量指数下降优于B、C组(P<0.05)。结论三种药物在有效降压的同时均可逆转左心室肥厚,厄贝沙坦对左心室肥厚的逆转作用相对更强。     

Blood pressure and left ventricular hypertrophy in patients on different peritoneal dialysis regimens.

OBJECTIVE: To examine the relation between the results of ambulatory 24-hour blood pressure monitoring (ABPM) and left ventricular mass index (LVMI), then to find the independent determinant for left ventricular hypertrophy (LVH) in peritoneal dialysis (PD) patients. Finally, to evaluate the differences in the clinical and cardiovascular characteristics between patients on continuous ambulatory PD (CAPD) and continuous cyclic PD (CCPD). DESIGN: An open, nonrandomized, cross-sectional study. SETTING: Divisions of nephrology and cardiology in a medical center. PATIENTS: Thirty-two uremic patients on maintenance PD therapy (22 patients on CAPD, and 10 on CCPD) without anatomical heart disease or history of receiving long-term hemodialysis. INTERVENTIONS: Home blood pressure (BP) and office BP were measured using the Korotkoff sound technique by sphygmomanometer. ABPM was employed for continuous measurement of BP. Echocardiography was performed for measurement of cardiac parameters and calculation of LVMI. MAIN OUTCOME MEASURES: Multivariate logistic regression analysis was performed for independent determinant of LVH in PD patients. The differences in clinical and cardiovascular characteristics between CAPD and CCPD patients were compared. RESULTS: Simple regression analysis showed positive correlations between LVMI and the duration of hypertension, ambulatory nighttime BP/BP load/BP load > 30%, serum phosphate, calcium-phosphate product, ultrafiltration (UF) volume, and percentage of UF volume during the nighttime. A negative correlation was noted between LVMI and dipping. In multiple regression analysis, the duration of hypertension was the only variable linked to LVMI. In multivariate logistic regression analysis, only ambulatory nighttime systolic BP load > 30% had an independent association with LVH.There were correlations between office/home BP and ambulatory 24-hour BP. In addition, CCPD patients had higher LVMI, UF volume during the nighttime, and percentage of UF volume during the nighttime than those of CAPD patients. CONCLUSIONS: In this study, ambulatory nighttime systolic BP load > 30% had an independent association with LVH. Office and home BP measurements were correlated with ABPM in PD patients. The result that CCPD patients had a higher LVMI than CAPD patients may be due to a relative volume overload during the daytime in CCPD patients.     

老年原发性高血压患者并发阵发性心房颤动的预测研究

目的 探讨老年原发性高血压患者并发阵发性心房颤动的预测因子。方法 87例老年原发性高血压患者分为两组。A组：并发阵发性心房颤动（PAF）的老年原发性高血压患者41例，B组：无PAF的老年原发性高血压患者46例；全部病例均进行同步12导联心电图、彩色多普勒超声心动图检查覆24h动态血压监测。结果 A组P波离散度（Pd）、P波最大时限（Pmax）、左心宣心肌重量指数（LVMI）、24h平均收缩压（24hSBP）、夜间平均收缩压（nSBP）均显著大于B组（均为P〈0．05）。Logistic逐步回归分析结果显示Pd、LVMI、nSBP均为老年原发性高血压患者并发PAF的独立预测因子（P〈0．05）。结论 Pd、LVMI、nSBP可以作为老年原发性高血压患者并发PAF的独立预测因子。     

Morphologic left ventricular patterns and prevalence of high-grade ventricular arrhythmias in the normotensive and hypertensive elderly

In the elderly, systemic hypertension is the main risk factor for cardiovascular diseases. Left ventricular hypertrophy, the most common adaptation to chronic pressure overload, has been recognized as an independent risk factor for an increased incidence of sudden death and arrhythmic disturbances. This study compared the prevalence of serious ventricular arrhythmias in elderly individuals with uncomplicated hypertension and in normotensive age-matched controls, using left ventricular mass index (LVMI) to differentiate patterns of anatomic adaptation to systolic, diastolic, or systolic-diastolic hypertension. The study enrolled 378 con-secutive untreated elderly subjects (≥65 years of age), without clinical evidence of heart failure; 203 were hypertensive and 175 were normotensive. Each participant underwent standard 12-lead electrocardiography, M-mode and B-mode echocardiography, and 24-hour ambulatory electrocardiographic monitoring. Serious, statistically significant arrhythmias (Lown classes ≥3) were present in 6.8% of normal subjects versus 17.1% of individuals with systolic, 31.5% of those with diastolic, and 20.4% of participants with systolic-diastolic hypertension. Arrhythmias did not differ in terms of left ventricular morphologic patterns or LVMI or between subgroups of hypertensive patients. Our data support the hypothesis that the pathogenesis of arrhythmias is related not to the electrophysiologic derangement of hypertrophied muscle but, rather, to the effects of hypertension on the cardiac structure. Cardiac fibrosis, one of the deleterious events accompanying hypertension, may be the main substrate for ventricular arrhythmias.