高血压左心室肥厚与血浆甲状旁腺升压因子的关系

目的观察高血压患者左心室肥厚与血浆甲状旁腺升压因子(PHF)的关系。方法将60例高血压患者根据左心室质量指数[LVMI＞125g/m2(男),＞120g/m     

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     

血浆甲状旁腺激素与高血压左室肥厚的关系

血浆甲状旁腺激素与高血压左室肥厚的关系惠永明陈新根王策西华（电力总医院心内科，北京１０００７３）ＰａｒａｔｈｏｒｍｏｎｅａｎｄＶｅｎｔｒｉｃｕｌａｒＨｙｐｅｒｔｒｏｐｈｙｉｎＥｓｓｅｎｔｉａｌＨｙｐｅｒｔｅｎｓｉｏｎＨｕｉＹｏｎｇｍｉｎｇ，ＣｈｅｎＸ...     

透析患者甲状旁腺机能亢进与左心室肥厚的关系

目的　了解透析患者甲状旁腺机能亢进与左心室肥厚 (L VH)的相关关系。方法　分别测量我院 46例腹膜透析 (CAPD)患者、73例血液透析 (HD)患者、18例透析前慢性肾衰竭患者及 16例健康人的超声心动图 ,以了解左心室肥厚的发生率 ,并分别检查血甲状旁腺素 (i PTH)、钙、磷水平 ,分析血钙、磷、i PTH与 L VH之间的关系。结果　CAPD组、HD组、肾衰竭组的 i PTH较对照组明显增高 (P<0 .0 0 1) ,以肾衰竭组升高明显 ,并且与 L VH呈显著正相关 (r=0 .70 5 ,P<0 .0 0 1)。 CAPD组、HD组的血钙值、血磷值与对照组无明显差别 ,而慢性肾衰竭组则血钙明显低下、血磷明显升高。结论　尿毒症患者普遍存在甲状旁腺机能亢进 ,是导致透析患者心血管疾病发病率增高的原因之一     

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.     

老年高血压左心室肥厚与心律失常关系的探讨

冠心病是引起心律失常的首要病因.然而目前的研究发现,在老年病人中高血压所导致心律失常的发生率并不低.有关资料表明,老年高血压组较正常对照组有较高的总房性、室性心律失常及短阵房性心动过速或心房颤动和Lown氏分级≥3级室性心律失常[1],而且老年高血压伴左心室肥厚者(Left VentricularHypertrophv,LVH),其总房性心律失常和Lown氏分级≥3级室性心律失常发生率明显高于不伴LVH者,提示老年高血压LVH与心律失常的发生密切相关[2,3].     

原发性高血压左心室肥厚与心律失常的关系

目的探讨原发性高血压(EH)病人左心室肥厚(LVH)与心律失常的关系.方法采用24 h动态心电图(DCG)、超声心动图(UCG)对156例EH病人进行检查并分组分析.结果LVH组室性心律失常和复杂室性心律失常的发生率显著高于非LVH组(P＜0.01);房性心律失常的发生率显著高于室性心律失常(P＜0.01).结论左心室肥厚是导致室性心律失常的危险因素之一.     

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。     

高血压左心室肥厚与心室晚电位的关系

检测100例高血压患者和60例正常血压组LVM、LV-MI及LP、VP、VT。结果显示LP阳性检出率高血压组与正常血压组分别为16.0%与1.6％（P＜0.001），高血压组LVH与无LVH者，LP阳性检出率分别为26.7％与7.2％（P＜0.01）。表明高血压组LVH者LP和VP、VT阳性检出率均明显高于无LVH者和正常血压组，提示LP与高血压LVH者的VP、VT密切相关。     

老年高血压患者血压变异性与左室肥厚的关系

目的 探讨老年高血原病患者血压变异性（BPV）与左室肥厚的关系。方法 选择216例高血压患者进行24h动态血压监测（ABPM）和超声心动图检查，分析血压变异性与左室肥厚的关系。结果 老年高血压患者合并左室肥厚组与无左室肥厚组比较，年龄、性别、24h平均血压和血糖、血脂水平无显著差异，但左室肥厚组的24h收缩压变异性（16．8±1．9VS14．3±2．3），白昼（14．9±2．5VS13．8±2．4）和夜间（10．8±3．7VS9．7±2．9）收缩压变异性均显著大于无左室肥厚组（P〈0．05）。结论 老年高血斥患者收缩斥波动与左室肥厚密切相关，可能预测高血压靶器官损害和不良心血管事件。     

日间血压变异与高血压患者左心室肥厚的相关性

目的:探讨日间血压变异性(blood pressure variability,BPV)与高血压患者左心室肥厚的相关性。方法:入选2013年11月至2014年1月于心内科及神经内科住院的高血压患者183例,连续监测血压6 d,以收缩压(SBP)值的标准差作为日间BPV的评估指标,将患者分为2组:BPV≥8.62 mmHg组、BPV8.62 mmHg组,收集患者的临床资料,进一步探讨日间BPV与左心室肥厚的关系。结果:(1)与日间BPV8.62 mmHg的患者相比,日间BPV≥8.62 mmHg的患者脑卒中患病率、SBP、舒张压、低密度脂蛋白胆固醇水平、尿蛋白阳性率、左心室后壁厚度、左心室质量指数(left ventricular mass index,LVMI)明显增高,低脂饮食的比例、平均睡眠时间较低(P0.05);(2)多元线性回归分析显示,在校正了多个混杂因素后,日间BPV与LVMI呈正相关。结论:日间BPV高的患者临床状况较差,日间BPV高是左心室肥厚的独立危险因素。     

Inter-atrial conduction time shortens after blood pressure control in hypertensive patients with left ventricular hypertrophy

Assuming that blood pressure control could induce a shortening of the inter-atrial conduction time and prevent atrial fibrillation occurrence, we studied the inter-atrial conduction time in hypertensive patients with left ventricular hypertrophy. METHODS: Sixty-eight (26 male) 58.34+/-8.08-year-old patient participated in the study. All were in sinus rhythm and had abnormal blood pressure (163+/-18/95+/-9 mm Hg). Their cardiac mass index was increased (151+/-43 g/m(2) SC) and their left atrial dimension was normal (3.67+/-0.54 cm). The inter-atrial conduction time was measured in the echocardiogram from the beginning of the electrocardiographic P wave to the beginning of the A wave in the mitral Doppler signal and was corrected for heart rate. Heart rhythm disturbances were monitored clinically and by means of a Holter. Most patients were treated with angiotensin antagonists. RESULTS: It was found that arterial blood pressure decreased significantly after treatment and that the P-A interval was significantly reduced (71.4+/-14.5 vs. 63.9+/-11.5 ms). During the follow-up, no patient complained of arrhythmia symptoms or exhibited atrial fibrillation in the Holter recording. CONCLUSION: In this selected group of patients with hypertensive heart disease (left ventricular hypertrophy), an effective blood pressure control was accompanied by a significant decrease in the inter-atrial conduction time. It is possible that these effects prevent atrial fibrillation.     

Ambulatory blood pressure and left ventricular hypertrophy

The relation between ambulatory blood pressure and left ventricular mass has been studied with three main aims. The first aim was to validate this new technique for measuring blood pressure. Most studies have shown that the left ventricular mass is correlated more closely to the ambulatory blood pressure than it is to the office blood pressure. The second aim was to define the parameters of most interest in ambulatory recordings. Although the mean 24 h blood pressure has emerged as the parameter of most clinical interest, other parameters, such as the blood pressure measured during activity, the difference between daytime and night-time values and the blood pressure measured when the subject arises in the morning, may also be of value. The interest of these parameters awaits confirmation in prospective studies. Random peak pressures and the variability as determined by discontinuous measurements using non-invasive methods appear to be of little value. The third aim was to assess the value of ambulatory monitoring in identifying the role played by mechanical as opposed to genetic, humoural and hormonal factors in the development of left ventricular hypertrophy in the hypertensive patient. Ambulatory blood pressure monitoring might prove of particular value in assessing the true impact of blood pressure reduction by antihypertensive therapy on left ventricular hypertrophy.     

Correlations between blood pressure, left ventricular hypertrophy, and left ventricular diastolic function in hypertensive patients]

We examined the relationship of hypertension to left ventricular hypertrophy (LVH) and left ventricular diastolic function by ambulatory blood pressure monitoring device and echocardiography. We studied 36 untreated hypertensive non-diabetic patients (16 males and 20 females) whose casual systolic blood pressure (CSBP) and/or diastolic blood pressure (CDBP) were higher than 140 mmHg and 90 mmHg, respectively. All patients were less than 65 years of age without organic heart disease. Resting systolic and diastolic blood pressures (RSBP, RDBP) were measured after lying in a supine position for 30 min by the auscultatory method. Ambulatory blood pressure was measured every 30 or 60 min for 24 hours by Colin ABPM 630, and the mean 24-hour ambulatory systolic and diastolic blood pressures (ASBP, ADBP) and the systolic and diastolic hyperbaric indices (SHI, DHI) were obtained. The left ventricular mass index (LVMI) was obtained as an indicator of LVH by M-mode echocardiography. The ratio of peak velocity of mitral inflow caused by atrial contraction to that of rapid inflow (A/R) was obtained as an indicator of the LV diastolic function by Doppler echocardiography. The coefficients of correlation between BP and the LVMI, and the A/R were determined. There were significant positive correlations between the LVMI and ASBP (r = 0.51, p < 0.005), the SHI (r = 0.49, p < 0.005), CSBP (r = 0.47, p < 0.01) and RSBP (r = 0.41, p < 0.05), however, there were no significant correlations between the LVMI and ADBP, the DHI, CDBP, RDBP and age. There were significant positive correlations between the A/R and ADBP (r = 0.44, p < 0.01), age (r = 0.40, p < 0.02), CSBP (r = 0.38, p < 0.05) and RDBP (r = 0.38, p < 0.05), however, no significant correlations between the A/R and ASBP, the SHI, DHI, RSBP and CDBP. Only a weak correlation was observed in all subjects between the LVMI and A/R, which was slightly improved by use of > 90 mmHg CSBP readings (r = 0.32). It was concluded that LVH is related mainly to continuous systolic hypertension, and that LV diastolic dysfunction is related mainly to continuous diastolic hypertension. Therefore, it was suggested that LVH and LV diastolic dysfunction in hypertensive patients are caused by different mechanisms.     

Angiotensin II stimulates left ventricular hypertrophy in hypertensive patients independently of blood pressure

Angiotensin II (AII) is known to be a growth stimulating factor for myocardial cells. We examined whether an exaggerated responsiveness to AII might aggravate left ventricular (LV) hypertrophy in human essential hypertension. To determine the responsiveness to AII in humans, we examined changes in mean arterial pressure (MAP), renal blood flow (RBF), and glomerular filtration rate (GFR) (steady state input clearance technique with para-aminohippurate and inulin, respectively) and aldosterone secretion to AII infusions (0.5 and 3.0 ng/kg/min) in 71 normotensive male and 48 hypertensive male subjects (age: 26 ± 3 years; 24-h ambulatory blood pressure: 121 ± 5/71 ± 4 mmHg v 138 ± 7/82 ± 7 mmHg, P < .001). In addition, each patient underwent two-dimensional guided M-mode echocardiography at rest to assess cardiac structure and function. When given AII 3.0, a greater increase of MAP (13 ± 7 v 17 ± 8 mm Hg, P < .022) and a more marked decrease of RBF (−203 ± 123 mL/min v −270 ± 137 mL/min, P < .007) were found in hypertensives than in normotensives, whereas changes in GFR and aldosterone concentration were similar in both groups. Most important, changes in GFR to AII correlated with echocardiographically determined LV mass (normotensives: AII 0.5: r = 0.33, P < .006, AII 3.0: r = 0.28, P < .05; hypertensives: AII 0.5: r = 0.41, P < .006, AII 3.0: r = 0.32, P < .05). After taking baseline MAP and body mass index into account, the increase in GFR to AII 0.5 in hypertensives still correlated with LV mass (partial r = 0.37, P < .01). Inasmuch as the increase of GFR is a marker of the responsiveness to AII (related to vasoconstriction at the postglomerular site), our data suggest that increased sensitivity to AII is linked to LV hypertrophy in early essential hypertension, independently of the level of blood pressure.     

高血压病左室肥厚患者心率变异及动态血压分析

观察高血压左室肥厚（ＬＶＨ）患者的心率变异（ＨＲＶ）及血压昼夜节律变化，以期了解三者之间的关系。选择伴有左心室肥厚的高血压病患者２１例，不伴有左心室肥厚的高血压患者２８例，选择年龄与患者可比的健康人２５例作为正常对照组，进行动态心电图及动态血压监测，分析２４ｈＨＲＶ时域指标及血压昼夜节律。结果:高血压伴左室肥厚患者ＨＲＶ各指标均显著低于对照组（Ｐ＜０．０５），也比不伴左室肥厚患者进一步降低。ＰＮＮ５０昼夜节律明显减弱。动态血压结果显示:不伴左室肥厚组与左室肥厚组血压昼夜节律消失者分别占各组总数的１７．９％及４７．６％，组间比较差异显著（Ｐ＜０．０５）。结论:副交感神经调节功能减弱可能与以上变化相关。高血压治疗应注意改善ＨＲＶ，重视恢复血压的昼夜节律     

脂联素水平与高血压左心室肥厚关系探讨

目的:探讨血清脂联素(APN)与高血压左心室肥厚(LVH)的关系。方法:高血压患者119例,经超声心动图检查,依据左心室质量指数(LVMI)划分为LVH组(60例)、非LVH组(59例)。采用酶联免疫分析方法测定血清APN浓度。依据血清APN水平将患者分为低水平组(5.5μg/mL)39例、中间水平组(5.5～7.4μg/mL)40例及高水平组(7.4μg/mL)40例,应用Logistic回归分析探究血清APN水平与LVH的关系。结果:LVH组血清Log-APN水平显著低于非LVH组〔(0.7±0.1)vs(0.9±0.1)〕μg/mL,(P0.001)。Logistic回归分析显示与高水平组比较,低水平组发生LVH的OR值为8.56(95%CI:2.51～29.18,P=0.001),中间水平组发生LVH的OR值差异无统计学意义。结论:低APN血症与高血压患者发生LVH相关。     

原发性高血压病人QT间期离散度与左室肥厚关系研究

目的：探讨原发性高血压病人左室重量与QT间期离散度的关系。方法：测定82例原发性高血压病人血压,计算QT间期离散度（QTcd)及QTcd%变化与左室重量指数（LVMI）的关系,结果：高血压伴左室肥厚（LVH）组的QTcd及QTcd^均明显高于无LVH组的;QTcd及QTcd%随LVMI增高而增高（r=0.7718,r=0.6798),但与血压无明显相关性,结论：高血压病人QTcd的增加不是血压变化结果,而是左室肥厚所致。