高血压左室构型与心功能的关系

目的与方法本文采用二维和Ｍ型超声心动图方法,将２０９例高血压病人的左室构型与心功能进行比较。结果正常左室构型组、向心性重构组中,心功能Ⅰ级的百分比分别为７５．４％和６０．０％,向心性肥厚组及离心性肥厚组心功能Ⅰ级仅占１２．７％和１１．８％;向心性肥厚组左房明显增大（提示左室顺应性下降）,而离心性肥厚组左室收缩功能明显下降。结论临床上对不同的左室构型应采取不同的治疗措施     

高血压患者左室构型改变与心功能的关系

目的探讨高血压患者左心室构型改变对心功能的影响。方法对高血压组164例和正常对照组30名进行常规心脏超声、心脏收缩功能和舒张功能检查。按Gnanu分类法将高血压组划分为正常构型组、向心性重构组、向心性肥厚组和离心性肥厚组。结果 E/A值在正常构型、向心性重构组、向心性肥厚组依次降低,在离心性肥厚组反而增高,舒张早期减速度(EDT)、等容舒张时间(IVRT)在高血压各组无统计学意义(P0.05);左心室短轴缩短率(FS)、左室射血分数(EF)在离心性肥厚组降低;心搏量(SV)、心输出量(CO)在正常构型、向心性重构组中无明显变化,而向心性重构组稍降低,离心性肥厚组稍增加;高血压各组Tei指数较正常对照组增高,在正常构型、向心性重构组、向心性肥厚组和离心性肥厚组呈依次增高,离心性肥厚组的Tei指数最高。结论高血压不同左室构型可引起左室收缩、舒张功能不同程度损害,以舒张功能障碍先于收缩功能障碍。而收缩功能受损以离心性肥厚组为明显。临床上应有效控制其构型的发展可从根本上减少心血管事件的发生率和病死率。     

高血压左室构型与左室中层力学的关系

目的：用室壁应力－左室中层缩短率关系做为评价心肌收缩性的指标,研究高血压不同左室构患者心肌收缩性的改变与心功能变化的关系。方法：应用超声心动图计算左室重量指数（ＬＶＭＩ）和相对室壁厚度（ＲＷＴ）,按ＬＶＭＩ和ＲＷＴ将左心室分为四种构型。对１１７例原发性高血压病人和４５例健康人左心室结构按左室室壁应力（ＭＥＳＳ）和室壁中层缩短率（ｍＦＳ）来估计心功能情况。结果：以射血分数、左室短轴缩短率和左室中层缩短率表示的收缩功能离心性肥厚受损严重,以室壁应力－左室中层缩短率关系表示的心肌收缩性,向心性肥厚最重。以ＥＦ斜率等表示的心脏舒张功能高血压不同左室构型患者损害不同,舒张功能的改变与心肌收缩必的损害成正相关。结论：高血压不同左室构型患者心肌收缩性损害不同,左室构型向向心性发展在一定阶段上代偿了心肌收缩性的下降,以保持心脏     

老年高血压性肥厚性心肌病8例报告

根据Ｔｏｐｏｌ提出老年高血压性肥厚性心肌病的概述报道一组具有高血压病史且有严重的左心室向心性肥厚，左室腔径缩小，收缩功能增加，舒张功能受损等特点崦不同于一般的高心病和原发性肥厚性心肌病的老年患者。患者究竟属高心病的一个特殊类型还是肥厚性心肌病患者伴有高血压，上前尚未定论。     

相对室壁厚度对原发性高血压患者左室功能的预测作用

目的采用超声指标评价原发性高血压患者不同左室几何构型的左室功能,探讨相对室壁厚度（RWT）与左室收缩功能和舒张功能的关系。方法利用超声心动图观察24名健康成年人和120例原发性高血压患者,根据RWT和左室重量指数（LVMI）将高血压患者分为四种左室几何构型组,分别以室壁中层缩短率（mFs）及E/A比值来评价左室收缩及舒张功能。应用单因素方差分析比较不同组间各参数的差异,应用多元回归分析分别筛选与mFs及E/A比值独立相关的参数。结果与正常对照组比较、左室正常构型组比较,向心性重构组和向心性肥厚组mFs明显降低（P〈0.01）;在多元回归分析中,RWT分别与mFs和E/A比值独立相关（r2=0.67,P〈0.01;r2=0.27,P〈0.01）。结论原发性高血压患者向心性重构组和向心性肥厚组左室收缩功能和舒张功能受损明显。RWT对原发性高血压患者左室收缩功能和舒张功能具有预测作用。     

老年高血压左室肥厚与舒张功能的关系

目的探讨老年高血压病患者左室肥厚（ＬＶＨ）与舒张功能的关系。方法６０例老年高血压病患者经二维超声检查分为ＬＶＨ组及无ＬＶＨ组，并设对照组（无高血压者）。用脉冲式多普勒分别测定二尖瓣舒张早期血流充盈峰值（ＰＶＥ）、舒张晚期充盈峰值（ＰＶＡ）及ＰＶＡ／ＰＶＥ以评价左室舒张功能。全部数据用ｘ±ｓ表示，组间差异用ｔ检验，指标间相关关系用直线相关求出并进行相关系数显著性检验。Ｐ＜０．０５为判断差异有显著性的标准。结果老年高血压病患者左室心肌重量指数（ＬＶＭＩ）增加、左房增大、左室舒张功能受损。且ＬＶＭＩ增加与左室舒张功能受损有关。结论老年高血压病患者左室舒张功能受损先于收缩功能受损。而且，左室舒张功能受损并非ＬＶＨ所致，但ＬＶＨ可加重左室舒张功能受损。左房（ＬＡ）增大是左室舒张功能受损的代偿结果。     

高血压左室构型与左室中层力学的关系

目的:用室壁应力-左室中层缩短率关系做为评价心肌收缩性的指标,研究高血压不同左室构型患者心肌收缩性的改变与心功能变化的关系.方法:应用超声心动图计算左室重量指数(LVMI)和相对室壁厚度(RWT),按LVMI和RWT将左心室分为四种构型.对117例原发性高血压病人和45例健康人左心室结构按左室室壁应力(MESS)和室壁中层缩短率(mFS)来估计心功能情况.结果:以射血分数、左室短轴缩短率和左室中层缩短率表示的收缩功能离心性肥厚受损最重,以室壁应力-左室中层缩短率关系表示的心肌收缩性,向心性肥厚最重.以EF斜率等表示的心脏舒张功能高血压不同左室构型患者损害不同,舒张功能的改变与心肌收缩性的损害成正相关.结论:高血压不同左室构型患者心肌收缩性损害不同,左室构型向向心性发展在一定阶段上代偿了心肌收缩性的下降,以保持心脏收缩排血功能的正常.     

高血压左心室重构及对心脏功能的影响

102例原发性高血压患者,以彩色多普勒超声心动图检查结果为基础进行分组研究,并与34例正常组对照,发现高血压组左心室重构,且左心功能与对照组明显不同(P<0.01).高血压心室重构早期左心房增大,继之室壁向心性对称性肥厚,最后左室内径容积扩大,这种心室重构的变化与高血压的程度和持续时间呈正相关.左室形态的变化使心室不能正常的舒缓,顺应性降低,舒张功能首先受损.随着室壁应力的过度增加,舒张功能进一步恶化,收缩功能降低.     

左室舒张功能衰竭药物治疗的新观念

近年来,对左室舒张功能衰竭的治疗日益受到重视。左室收缩和舒张不全是相互关联的,以往对心室充盈受限、充盈增高为特征的“舒张功能衰竭”缺乏认识。临床上约有1/3的充血性心力衰竭患者心脏收缩功能测指标无明显异常,某些正性肌力药物无明显改善心功能作用,此类心衰常称之为以舒张功能障碍为主的心衰。其常见病因有高血压,冠心病和肥厚性心肌病     

左室舒张功能衰竭药物治疗的新观念

近年来．对左室舒张功能衰竭的治疗日益受到重视。左室收缩和舒张不全是相互关联的．以往对心室充盈受限、充盈增高为特征的“舒张功能衰竭”缺乏认识。临床上约有1/3的充血性心力衰竭患心脏收缩功能测指标无明显异常．某些正性肌力药物无明显改善心功能作用，此类心衰常称之为以舒张功能障碍为主的心衰。其常见病因有高血压．冠心病和肥厚性心肌病等。病理改变为：左室壁增厚、僵硬度增加，心肌缺血或退行性变，二尖瓣、主动脉瓣增厚纤维化或钙化．心肌纤维中ATP酶活性及内生肾上腺素含量发生改变心肌收缩与舒张不协调，收缩及舒张速率下降。     

高血压患者左室重构与心功能及心律失常关系

研究高血压患者左室重构对心律失常及心功能影响。方法应用多普勒超过心动图声学定量技术和动态心电图检测８７例高血压压患者。结论左室重构对高血压早期左室收缩功能有一定代偿作用,但随着心室重构、左室肥大,心脏功能损害更加明显,同时心室重构明显增加室性心律失常的发生。     

原发性高血压患者心脏结构和功能改变的流行病学调查

目的:了解北京市合并原发性高血压的住院患者心脏结构和功能改变的特点及相关因素。方法:针对北京地区4 081例原发性高血压住院患者进行流行病学回顾性调查,超声指标包括左心房及左心室内径,室间隔和左心室后壁厚度,E／A比值和左心室射血分数。其他指标包括患者的一般情况、病史和治疗情况。结果:高血压患者左心房扩大和E／A比值异常分别占所有患者的50．6％和70．0％,是高血压心脏损害最常见的两种表现。60～79岁老年人合并各种心脏结构和功能异常的比例均高于中年人。左心房扩大和左心室肥厚呈现出随血压水平升高,异常率增加的趋势。合并心脏结构和功能损害的高血压患者更多的使用联合用药。多因素分析显示,与左心房扩大有关的危险因素有合并心房颤动、肥胖、高龄、高血压病程长以及收缩压增高。与左心室肥厚有关的危险因素同样有高血压病程长、收缩压增高和高龄。与左心室扩大有关的危险因素有女性、合并心房颤动和肥胖。结论:①左心房扩大和E／A比值异常是高血压心脏损害最常见的两种表现;②老年人合并更多的心脏结构和功能损害;③血压水平越高,合并左心房扩大和左心室肥厚者越多;④男性、高血压病程长、收缩压增高和高龄是左心房扩大和左心室肥厚共同的危险因素,合并心房颤动患者合并更多的左心房扩大和左心室扩大。     

Influence of plasma aldosterone on left ventricular geometry and diastolic function in treated essential hypertension.

Since aldosterone is known to promote interstitial fibrosis in cardiac tissues, it is possible that aldosterone may influence cardiac structure and function. In the present study, we investigated whether plasma aldosterone concentration (PAC) is related to the distinct patterns of left ventricular (LV) geometry and LV diastolic function in treated essential hypertension. In 92 patients with chronically treated essential hypertension, two-dimensional and Doppler echocardiographic examinations were performed and LV inflow velocities were measured for evaluation of LV diastolic function. When patients were divided into four groups by the different LV geometric patterns, PAC in patients with eccentric hypertrophy was significantly higher than in those with concentric hypertrophy (15.2+/-2.1 vs. 10.0+/-0.7 ng/dl, p<0.01). However, the ratio of the peak velocity of early diastolic filling to that of atrial filling (EIA), an index of LV diastolic function, was significantly decreased in patients with concentric hypertrophy compared with those showing normal geometry. In the relationship between PAC and LV diastolic function, PAC was negatively correlated with EIA (r=-0.35, p<0.05) only in the subgroup with normal relative wall thickness (i.e., without the concentric change in LV geometry). A multiple linear regression analysis showed that PAC was one of the independent determinants of E/A in the overall subject group. These observations indicate that PAC is associated with the eccentric change in LV geometry in patients with treated essential hypertension and also suggest that the increase in PAC participates in the impairment of LV diastolic function apart from the concentric change in LV geometry, although concentric hypertrophy clearly impairs LV diastolic function.     

Left ventricular hypertrophy and geometry in a population sample of elderly males

BACKGROUND: Recent studies have shown that left ventricular geometric adaptationto hypertension is complex. The spectrum of geometric adaptationsin a general population and its relationship to systolic anddiastolic function has, however, not been investigated. OBJECTIVES AND METHODS: This echocardiographic and Doppler study investigated the relationshipsbetween left ventricular geometric shape (normal, concentricremodelling, concentric hypertrophy and eccentric hypertrophy)and left ventricular systolic and diastolic function in a populationsample of 584 males aged 70 in Uppsala, Sweden. The influencesof hypertension, coronary heart disease and diabetes mellituswere also evaluated. RESULTS: Sixteen percent of the healthy population (n=167) demonstratedthe presence of left ventricular hypertrophy (mainly eccentric).Subjects with hypertension (n=115) showed an increased leftventricular mass (eccentric left ventricular hypertrophy 31%,concentric left ventricular hypertrophy 15%), when comparedwith healthy subjects (P<0.001). Subjects with coronary heartdisease (n=32) without hypertension also showed an increasedleft ventricular mass (most often eccentric) (P<0.05). UsingDoppler determinations of cardiac index, no differences werefound in cardiac index between the geometric groups. Raisedtotal peripheral resistance, increased blood pressure and enlargedleft atrium were found in both concentric and eccentric leftventricular hypertrophy (P<0.01–0.05). Disturbed diastolicfunction was seen with a prolongation of the isovolumic relaxationtime in eccentric (P<0.01) and increased atrial-dependentleft ventricular filling in concentric left ventricular hypertrophy(P<0.05). CONCLUSIONS: Alterations in left ventricular geometry were common in thispopulation-based study of elderly males, both in healthy subjectsand in subjects with hypertension or coronary heart disease.Raised total peripheral resistance and left ventricular diastolicdysfunction were common findings in both concentric and eccentricleft ventricular hypertrophy.     

Cardiac performance and morphology in end-stage renal disease

Patients with end-stage renal disease (ESRD) experience a variety of hemodynamic and metabolic abnormalities that predispose to alterations in cardiac performance and morphology. High cardiac output related to renal anemia, hypertension, volume overload, and the arteriovenous fistula (in patients on hemodialysis) predispose to eccentric left ventricular (LV) hypertrophy. Hypertension, aortic stiffness, and aortic stenosis predispose to concentric LV hypertrophy. Most ESRD patients have a hybrid form of LV hypertrophy. LV hypertrophy is commonly accompanied by LV diastolic dysfunction. LV systolic dysfunction is less common. Newer dialytic techniques, excellent control of hypertension, and correction of renal anemia produce regression of LV hypertrophy. The effect of these interventions on LV systolic and diastolic function is less well established. Alterations in serum calcium, choice of dialysate base, hypoxia, and comorbid conditions may influence the effects of dialysis (particularly hemodialysis) on LV function. A variety of negative inotropic drugs may depress LV function in patients with ESRD.     

Quantification of the contribution of cardiac and arterial remodeling to hypertension

The study aim was to quantify the individual and combined contributions of both the arterial system and the heart to systolic blood pressure in hypertension. We assessed the parameters of a heart-arterial model for normotensive control subjects and hypertensive patients with left ventricular adaptation patterns classified as normal, concentric remodeling, concentric hypertrophy, or eccentric hypertrophy. The present simulations show that vascular stiffening alone increases the pulse pressure without increasing systolic blood pressure. It is only in combination with an increased peripheral resistance that arterial stiffening leads to systolic hypertension in concentric remodeling and concentric hypertrophy. The contribution of cardiac pump function to the increase in blood pressure depends on cardiac remodeling, hypertrophy, or both. In hypertensive patients with a normal left ventricle, the heart is responsible for 55% of the increase in systolic blood pressure. In concentric remodeling, concentric hypertrophy, and eccentric hypertrophy, the cardiac contribution to the increase in systolic blood pressure is 21%, 65%, and 108%, respectively. We conclude that along with arterial changes, cardiac remodeling and hypertrophy contribute to hypertension.     

Longitudinal global and regional left ventricular function in patients with hypertensive disease (tissue Doppler echocardiography data)

Impulse tissue doppler study was carried out in 154 patients with hypertensive disease (age 35-60 years) and 39 practically healthy volunteers (mean age 43.4+/-5.5 years). According to left ventricular geometry the following groups of patients were distinguished (after A.Ganau): with normal geometry (n=47), with concentric remodeling (n=12), with concentric hypertrophy (n=53), and with eccentric hypertrophy (n=42). Tissue doppler spectrum was registered from mitral annulus and 15 left ventricular segments. The following characteristics were obtained: in each annular spectrum - maximal velocities of peaks s(m), e(m), a(m), ratio e(m)/a(m), isovolumic relaxation time (ivrt) and their average values (from 6 measurements); in each left ventricular segmental spectrum - maximal velocities of waves s, e, a, ratio e/a and segmental ivrt. Compared with healthy persons patients with hypertension had lowered longitudinal global systolic function of the left ventricle. Patients with concentric left ventricular hypertrophy had least values of e(m), e(m)/a(m), ivrt(m) and greatest number of dysfunctional (e/a<1.0 and ivrt>90 ms) segments. Some hypertensive patients with normal values of transmitral blood flow had signs of segmental diastolic dysfunction. Among patients with normal left ventricular geometry isolated segmental diastolic dysfunction was revealed according to e/a in 12 of 20 (60%), according to ivrt in 11 of 22 (50%). All patients with concentric and eccentric left ventricular hypertrophy had segmental diastolic dysfunction. Thus impulse tissue doppler study is indicated to patients with hypertension and normal parameters of transmitral flow for assessment of longitudinal segmental diastolic left ventricular function.     

Variations in cardiac diastolic function in hypertensive patients with different left ventricular geometric patterns.

To evaluate the alteration of cardiac function in hypertensive patients with different left ventricular geometric patterns. Echocardiography was used to study left ventricular geometry and cardiac diastolic function in 117 cases of essential hypertension, with 45 normal cases as controls. Echocardiographic date were used to calculated the left ventricular mass index (LVMI) and relative wall thickness (RWT), which values in turn were used to divide the subjects into four groups. The left atrial dimension of the group, with the exception of these hypertensives who showed normal geometry, was larger than that of the control group. The damage of peak of E velocity, peak of A velocity, E/A and the slope between the E and F points (E to F slope) were greater than in hypertension than in the control group. The concentric hypertrophy group and eccentric hypertrophy group suffered more serious damage of left ventricular diastolic function than the concentric remodeling group, and damage of left ventricular diastolic function in the concentric remodeling group was greater than that in the normal geometry group. The degree of cardiac diastolic function damage differed among patients with different left ventricular geometric patterns, when the cardiac structure was changed, the degree of cardiac diastolic function damage increased.     

The influence of ambulatory blood pressure profile on left ventricular geometry

Besides causing a hypertrophy in the left ventricle, hypertension results in a change in the geometry of the left ventricle. The blood pressure, which does not decrease enough during the night, leads to structural changes in the left ventricle. In this study, the influence of 24-hour blood pressure profile on the left ventricular geometry was examined. Ambulatory blood pressure monitoring was applied to 60 patients with mild to moderate hypertension who had never been treated and standard echocardiographic evaluation was conducted thereafter. The patients were divided into two groups with respect to the ambulatory blood pressure profiles: the patients whose night blood pressure levels decreased by more than 10% compared to their daytime blood pressure levels (dipper) and those whose levels did not decrease that much (nondipper). The left ventricle mass index and the relative wall thickness of the patients were calculated. With respect to the left ventricle geometry, mass index and relative wall thickness of the patients were determined as: having normal geometry, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy. Age, gender, systolic, and diastolic blood pressure were similar within the dipper and nondipper groups. Normal geometry, concentric remodeling, and concentric hypertrophy ratios were similar in both groups. Eccentric hypertrophy was higher in the nondipper group compared to the dipper group (42.9% vs 6.3%, P < 0.03). Patients with mild to moderate hypertension, whose blood pressure does not decrease enough, develop eccentric hypertrophy.     

Cardiac hypertrophy due to pressure and volume overload: distinctly different biological phenomena?

Myocardial hypertrophy is a morphological adaptive response to chronic work overload imposed on the heart. It has been categorized into two distinct basic types: concentric hypertrophy, occurring in response to a sustained pressure overload in which wall thickness increases without chamber enlargement, and eccentric hypertrophy, in response to a chronic volume overload in which chamber volume enlarges without a relative increase in its wall thickness. It should be emphasized, in this context, that these adjectives are somewhat confusing, since the hypertrophy observed is not eccentric in the fashion often seen in the left ventricle of patients with hypertrophic cardiomyopathy. In fact, the hypertrophy is concentric in both instances, but is associated with an increase in chamber volume when described as eccentric, yet occurring with a maintained volume when said to be concentric. In rats made anemic by iron deficiency, the volume overloaded heart achieves an adaptive increase in mass characterized as hypertrophy occurring in the setting of dilated ventricle. This so-called eccentric hypertrophy depends on catecholamines as possible signals for myocardial growth, and progresses with preserved ultrastructure and contractile performance of the cardiac muscle. A gradually imposed volume overload results in a harmonious growth of the heart (it retains a relative normal shape, becoming a magnified normal heart), probably mediated by release of catecholamines into the myocardium. This process resembles the normal cardiac growth in response to the obligatory volume load imposed by an increasing cardiac output (greater metabolic demands) and blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)