北京市2671例住院老年高血压患者心脏损害及诊治情况的调查

目的了解北京市老年住院高血压患者的诊治情况以及心脏结构和功能改变的特点,为临床老年高血压的合理诊治提供依据。方法采用流行病学回顾性调查的方法,对60岁以上住院高血压患者的一般情况、病史、超声心动图结果和治疗情况等进行回顾性总结分析。结果共调查病例2671份,其中60～79岁的老年组2238例,≥80岁的老老年组男性383例。所有患者中仅660例（24.7%）未合并危险因素,1758例（65.8%）合并不同的心脏损害,545例（20.4%）合并不同部位的外周动脉硬化,631例（23.6%）合并脑血管病。老年组血压（146.40±24.28）/（81.87±13.31）mmHg,老老年组血压（143.91±21.83）/（76.85±11.93）mmHg。两组患者血压达标率（〈140/90mmHg）分别是33.3%和39.3%,尤以收缩压达标率差。老年高血压患者超声心动图显示存在多种心脏损害,其中E/A比值异常率高达77.3%。临床有心力衰竭表现的患者合并更多的心脏结构异常,包括左房扩大、左室扩大和左室肥厚,超声心动图更多的表现为舒张功能不全。结论（1）北京市住院老年高血压患者合并多种危险因素和靶器官损害;（2）北京市三级医院住院老年高血压患者血压控制率仍较低,尤以收缩压达标率低;（3）临床表现心功能不全的高血压患者超声更多显示心脏舒张功能异常。     

北京住院高血压患者心脏结构功能及治疗达标情况的分析

目的回顾性分析北京市三级医院住院的高血压患者的心脏结构功能改变的相关因素,为临床治疗提供依据。方法采用回顾性调查的方法,通过超声诊断技术分析高血压患者的心脏结构及功能的参数,并对患者的年龄、血压水平、合并的危险因素及疾病、降压药物使用情况进行相关分析。结果共分析住院的原发性高血压患者5106例,平均年龄63．78岁,平均血压145．97／84．23mmHg（1mmHg=0．133kPa）。75．5％的患者至少合并一种心血管危险因素,随着血压水平的升高,合并左心室肥厚的患者比例明显增高。有近30％的患者合并不同程度的心功能不全。调查中发现,左房扩大和左心室舒张功能不全是高血压患者最常见的心脏损害。多因素分析显示,较高的收缩压、舒张压、血肌酐水平、老年和低高密度脂蛋白胆固醇是高血压合并左心室肥厚的危险因素。所有患者血压达标率（血压〈140／90mmHg）为32．1％,单药治疗达标率为38．1％。钙拮抗剂和利尿剂是使用最多的两类降压药。结论要重视血压的治疗达标和多重危险因素共同干预以延缓或逆转高血压心脏损害的发生发展,原发性高血压的防治仍任重而道远。     

高血压患者心脏结构功能及临床治疗达标的研究

目的 探讨高血压患者的心脏结构功能改变的相关因素,为临床治疗提供依据.方法 采用回顾性调查方法,通过超声诊断技术分析高血压患者的心脏结构及功能的参数,对患者的年龄、血压水平、合并的危险因素及疾病、降压药物的使用情况进行相关分析.结果 随着血压水平的升高,合并左心室肥厚的患者比例明显升高.有近30.5%的患者合并不同程度的心功能不全.调查中发现,左心房扩大和左心室舒张功能不全是高血压患者最常见的心脏损害.所有患者血压的治疗达标率为30.8%,单药治疗达标率37.6%.结论 重视血压的治疗达标和多重危险因素共同干预以延缓和逆转高血压心脏损害的发生发展.     

原发性高血压患者左心房扩大及其影响因素

目的　分析 12 0例原发性高血压患者左心房大小及其影响因素。方法　原发性高血压患者 12 0例 ,男 5 9例 ,女 6 1例 ,年龄 33～ 78岁。全部患者分为两组 ,年龄≥ 6 0岁为老年组 (6 0例 ) ,年龄 <6 0岁为非老年组 (6 0例 )。每组根据心脏超声分为左心室肥厚和无左心室肥厚两个亚组。左心房内径大于 4cm为左心房扩大 ,面积 长度法左心室重量指数男性 >89g m2 ,女性 >77g m2 为左心室肥厚。结果　非老年组 4 3%、老年组 73%合并左心室肥厚 ;非老年组 14例 (2 3% )、老年组 2 2例 (37% )合并左心房扩大 ;37%患者左心房扩大和左心室肥厚同时并存 ,2 0 %患者仅有左心房扩大 ;两组左心房扩大者共 36例 ,其中老年组合并左心室肥厚占 5 0 % (18 36 ) ,非老年组合并左心室肥厚占 2 2 % (8 36 ) ;多因素分析提示超重、血压水平与左心房扩大无显著相关性 ,年龄和左心室重量指数同左心房扩大显著相关。结论　年龄与左心室肥厚是原发性高血压左心房扩大的重要影响因素。     

高龄老年患者动脉及心脏结构与功能变化

目的评价高龄老年患者动脉及心脏结构、功能变化。方法老年高血压或糖尿病患者分为两组,高龄组：80岁及以上,119例;老年组：60—79岁,78例。分别检测颈动脉内膜中层厚度（IMT）、冠状动脉钙化积分（CS）、动脉脉压（PP）;心脏超声检测室间隔厚度（IVS）、左室室壁厚度（LVPW）、舒张末期左心室内径（LVDd）、收缩末期左心室内径（LVDs）、收缩末期左心房前后径（LAD）、左室质量（LVM）、左室质量指数（LVMI）、左室射血分数（EF）、左心室舒张早期二尖瓣最大血流速度E峰及舒张晚期二尖瓣最大血流速度A峰比值（E／A）。结果高龄组冠脉钙化总积分（TCS）、右冠脉钙化积分（CSRCA）、IMT、PP、LVPW较老年组增高（P〈0．01）,E／A较老年组下降（P〈0．05）。结论老年期随增龄颈动脉内膜增生及左室肥厚进一步加重;高龄老人心脏舒张功能明湿下降,但对收缩功能影响不大;增龄导致的冠状动脉钙化更易侵犯右冠脉。     

老年原发性高血压患者左心房/左心室容量比值的变化

目的本文旨在探讨老年原发性高血压患者左心房容量／左心室容量比值变化的临床意义。方法老年正常对照组32例。老年原发性高血压无室壁肥厚患者35例，老年原发性高血压患者伴室壁肥厚者33例。应用实时三维三平面显像方式测量左房、左室容量，对3组病人的左房容量，左房内径，左房容量指数和左心房容量／左心室容量比值进行分析。结果左房容量，左房内径，左房容量指数和左心房容量／左心室容量比值在高血压室壁肥厚组与对照组之间均存在极显著差异（P〈0．01），但左房内径在原发高血压无室壁肥厚组与对照组之间无显著差异（P〉0．05）。左房容量、左房容量指数在原发高血压无室壁肥厚组与对照组之间差异有显著性（P〈0．05），左心房容量／左心室容量比值在原发高血压无室壁肥厚组与对照组之间差异更为显著（P〈0．01）且变异性最小。结论左心房容量／左心室容量比值是一种新的参数，能够灵敏地反映老年原发性高血压患者舒张功能减低的血流动力学改变。     

非酒精性脂肪性肝病与高血压患者心脏结构和功能的关系

目的探讨非酒精性脂肪性肝病(NAFLD)对高血压患者心脏结构和功能的影响。方法选取2016年10月-2019年12月期间诊疗的高血压患者345例作为研究对象,其中NAFLD合并高血压患者187例为观察组,单纯高血压患者158例为高血压组,另选同期健康体检者126人为对照组。比较3组受试者一般临床资料,超声测定左心室舒张末期内径、左心室舒张末期室间隔厚度、左心房前后径、左心室收缩末期内径、左心室射血分数、二尖瓣舒张期血流速度E峰和A峰及E/A值。采用Pearson相关性分析各指标与NAFLD的相关性,多因素分析采用多元线性回归分析。结果与对照组患者相比,高血压组患者的收缩压升高,高密度脂蛋白胆固醇水平降低,观察组患者体质量指数、腰围、收缩压、三酰甘油、总胆固醇、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶水平明显增高,高密度脂蛋白胆固醇水平降低,左心房前后径明显增高,左心室射血分数和E/A值降低(均P0.05)。与高血压组患者相比,观察组患者体质量指数、腰围、三酰甘油、总胆固醇、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶水平增高,高密度脂蛋白胆固醇水平降低,左心房前后径增高,左心室射血分数和E/A值降低(均P0.05)。Pearson相关性分析结果显示,腰围、γ-谷氨酰转肽酶、丙氨酸氨基转移酶、天冬氨酸氨基转移酶、左心房前后径、左心室射血分数、E/A值与NAFLD程度呈正相关(P0.05),HDL-C与NAFLD程度呈负相关(P0.05)。多元线性回归分析显示,高血压患者的左心房前后径、左心室射血分数、E/A值与NAFLD程度相关(P0.05)。结论 NAFLD可能加重高血压患者左心房增大、左心室收缩功能下降及舒张功能不全。     

高血压病对心脏左心房结构的影响

研究探讨了高血压病人左心房结构的改变与年龄、性别、高血压程度、高血压时间和左心室收缩舒、张功能之间的关系。方法：将２４１ 例高血压病人分别按年龄、性别、高血压程度和高血压时间分组，利用心动超声测量病人左心房面积、二尖瓣 Ｅ峰、 Ａ 峰、 Ｅ／ Ａ比值及 Ｅ Ｆ值，与正常组１０６ 例 分别进行统计学比较。结果：高血压病人左心房扩大的发生与年龄密切相关，与血压高度密切相关，与二尖瓣 Ｅ峰降低， Ａ 峰升高， Ｅ／ Ａ比值倒置的发生相一致，即左心房扩大与左心室充盈功能和顺应性密切相关。同时认为高血压病左房结构的改变与性别、高血压病程和左心室射血分数相关不密切。结论：左室充盈功能和顺应性降低是高血压病早期的改变，左心房扩大是高血压心脏病的早期征象。     

原发性高血压患者左心室肥厚与室性心律失常及心率变异性的关系

为探讨原发性高血压患者左心室肥厚与室性心律失常及心率变异性的关系。将原发性高血压患者分为无左心室肥厚组和左心室肥厚组，通过心脏B超观察原发性高血压患者心脏的结构与功能，通过动态心电图观察其24h室性期前收缩情况及心率变异性各时域指标。结果发现，左心室肥厚组患者的24h室性期前收缩发生率及室性期前收缩级别明显高于无左心室肥厚组（P＜0．01）；两组患者心率变异性各指标差异无显著性（P＞0．05）；与室性期前收缩级别相关的独立危险因素依次为室间隔厚度、左心室舒张末期内径和患者的年龄（P＜0．05，P＜0．001，P＜0．05）。以上提示原发性高血压合并左心室肥厚患者严重室性心律失常的发生率明显增高，而左心室肥厚与心率变异性无相关性。室间隔厚度、左心室舒张末期内径与年龄是原发性高血压患者发生室性心律失常的独立危险因素。     

原发性高血压患者左心房增大的相关因素分析

目的观察左心房增大在高血压人群中的发生率,初步探讨左心房增大的独立预测因素及相关机制。方法收集我院门诊或住院的1~2级原发性高血压患者156例,测定血压、血脂、血糖等,计算体重指数,所有患者接受超声心动图及颈动脉超声检查,检测左心房内径(>3.9 cm为左心房增大),将患者分为左心房增大组(36例)及左心房正常组(120例)。计算左心室重量指数,区分有无左心室肥厚。结果23%的患者存在左心房增大,与左心房正常组比较其年龄、病程、体重指数、甘油三酯、空腹血糖、左心室重量指数水平更高,高密度脂蛋白胆固醇水平更低,呈现左心室肥厚、颈动脉内膜增厚或斑块形成、代谢综合征的比例亦显著增高。logistic回归证实,超重(体重指数>25 kg/m2)、左心室肥厚、收缩压≥155 mm Hg(1 mm Hg=0.133 kPa),代谢综合征及颈动脉内膜增厚是预测左心房增大的独立因素。结论左心房增大与超重、左心室肥厚、代谢异常及颈动脉内膜增厚密切相关,可能是高血压病程中出现其他心血管及代谢异常时的适应性反应。     

Correlates of left atrial size in hypertensive patients with left ventricular hypertrophy: the Losartan Intervention For Endpoint Reduction in Hypertension (LIFE) Study

Left ventricular hypertrophy has been suggested to mediate the relation between hypertension and left atrial enlargement, with associated risks of atrial fibrillation and stroke. However, less is known about correlates of left atrial size in hypertensive patients with left ventricular hypertrophy. We assessed left atrial size by echocardiography in 941 hypertensive patients, age 55 to 80 (mean, 66) years, with electrocardiographic left ventricular hypertrophy at baseline in the Losartan Intervention For Endpoint reduction in hypertension study. Enlarged left atrial diameter (women, >3.8 cm; men, >4.2 cm) was present in 56% of women and 38% of men (P<0.01). Compared with the 512 patients with normal left atrial size, the 429 patients with enlarged left atrium more often had mitral regurgitation, atrial fibrillation, and echocardiographic left ventricular hypertrophy. They also had higher age, systolic blood pressure, pulse pressure, weight, body mass index, left ventricular internal chamber dimension, stroke volume, and mass and lower relative wall thickness and ejection fraction (all, P<0.05). In logistic regression analysis, left atrial enlargement was related to left ventricular hypertrophy and eccentric geometry; greater body mass index, systolic blood pressure, and age; female gender; mitral regurgitation; and atrial fibrillation (all, P<0.05). Thus, left atrial size in hypertensive patients with electrocardiographic left ventricular hypertrophy is influenced by gender, age, obesity, systolic blood pressure, and left ventricular geometry independently of left ventricular mass and presence of mitral regurgitation or atrial fibrillation.     

高血压患者脉压与左心室肥厚构型及心功能的关系

目的　探讨药物规则治疗下高血压病 (EH)患者的脉压 (PP)与左心室肥厚 (L VH)构型及心功能的关系。方法　本研究回顾性分析 176例有或无 L VH的 EH患者的 PP与 L VH构型及心功能的相关性。结果　 1不对称性室间隔肥厚 (ASH)、对称性室间隔肥厚 (CH)及扩张性肥厚 (DH)三型肥厚组的 PP与无 L VH组相比 ,有明显的差别 ,CH和 DH组较大 (P均 <0 .0 1) ,尤以 DH组较甚。2随着 PP增大 ,左心室收缩及舒张功能均明显的降低。3L ogistic回归分析显示 ,PP与 EH患者左心功能不全发生存在明显的相关性 ,PP每增加 10 m m Hg,左心功能不全增加 30 % (95 % CI:1.2 3～ 1.37,P<0 .0 0 0 1) ;在对年龄和 EH病程进行校正后 ,PP每增加 10 m m Hg显示增加左心功能不全发生率 19% (95 % CI:1.13～ 1.2 5 ,P<0 .0 0 0 1)。结论　在药物规则治疗的 EH患者中 ,PP与 L VH构型具有一定的联系 ,PP是左心功能不全发生的一个重要和独立的相关因素 ;且随着 PP增大 ,左心室收缩及舒张功能均明显的降低。     

Impaired left ventricular functional reserve in hypertensive patients with left ventricular hypertrophy

To determine whether patients with hypertension and especially those with left ventricular hypertrophy have subtle changes in cardiac function, we measured the increase in left ventricular ejection fraction and in systolic blood pressure to end-systolic volume index ratio with exercise in 40 hypertensive patients and 16 age-matched normotensive volunteers. Twenty-two hypertensive patients without hypertrophy had normal end-systolic wall stress at rest and exercise responses. In contrast, the 18 patients with echocardiographic criteria for left ventricular hypertrophy demonstrated a significant increase in end-systolic wall stress at rest compared with normal subjects (69 +/- 16 vs. 55 +/- 15 10(3) x dyne/cm2, p less than 0.05) despite having normal resting left ventricular size and ejection fraction. In patients with left ventricular hypertrophy, the increase in ejection fraction with exercise was less than in the normotensive control subjects (7 +/- 7 vs. 12 +/- 8 units, p less than 0.05), and delta systolic blood pressure to end-systolic volume with exercise was reduced (3.3 +/- 3.8 vs. 8.3 +/- 7.7 mm Hg/ml/m2, p less than 0.05). The hypertensive patients with hypertrophy displayed a shift downward and to the right in the relation between systolic blood pressure to end-systolic volume ratio and end-systolic wall stress compared with control subjects and hypertensive patients without left ventricular hypertrophy. Thus, hypertensive patients with left ventricular hypertrophy by echocardiography and normal resting ejection fraction exhibit abnormal ventricular functional responses to exercise. This finding may have implications in identifying patients at higher risk for developing heart failure.     

Left ventricular mass and blood pressure during ergometric exercise in primary hypertension

The pathophysiology of left ventricular hypertrophy (LVH) in hypertensive patients is still an intriguing point. The lack of a close relationship between LVH and systolic or diastolic blood pressure at rest, previously observed by other investigators, was confirmed in our group of 45 patients with uncomplicated primary hypertension. The strength of correlation between echocardiographic left ventricular mass (LVMe) and blood pressure, expressed as incremental area (IA = total area under the curve--basal area), however, increased during bicycle exercise testing (r = 0.33, p less than 0.05 for diastolic blood pressure; r = 0.39, p less than 0.01 for systolic blood pressure; r = 0.41, p less than 0.01 for mean arterial pressure). Other echocardiographic parameters of myocardial mass such as LVM index (LVMI) and septal thickness (ST) were also significantly correlated with blood pressure during exercise. These results suggest either that blood pressure during exercise is a better index of the cardiac workload than resting blood pressure or that the pathogenesis of cardiac hypertrophy involves an enhanced reactivity to adrenergic drive, particularly stimulated during ergometric exercise. Increased blood pressure alone, however, only partly accounts (about 20%) for the increase in myocardial mass in hypertensive patients; other factors, therefore, need to be further investigated for a better understanding of the pathophysiology of left ventricular hypertrophy.     

高血压合并糖尿病患者左心室肥大与血压变异性指数的相关性分析

目的研究高血压合并糖尿病患者左心室肥大与血压变异性(BPV)指数的相关性。方法纳入高血压合并糖尿病患者120例,并根据患者的临床确诊资料信息及心电图资料将患者分为左心室肥大(LVH)组和非LVH组,比较两组的BPV相关指数,Logistic回归分析患者左心室肥大的相关危险因素,Pearson相关分析左心室质量指数(LVMI)与BPV各指标之间的相关性。结果高血压合并糖尿病LVH组患者较非LVH组患者的白天收缩压变异系数(dSBPCV)、白天舒张压变异系数(dDBPCV)、24 h收缩压变异系数(24hSBPCV)、24 h舒张压变异系数(24hDBPCV)均显著上升(P<0.05);Logistic回归分析结果提示dSBPCV、dDBPCV、24hDPBCV、24hSBPCV水平的上升是高血压合并糖尿病患者左心室肥大的相关危险因素(OR>1,P<0.05);Pearson相关分析结果提示:LVMI与24hSBPCV、24hDBPCV以及dSBPCV、dDBPCV均呈正相关(r分别为0.345、0.412、0.387、0.441,P<0.05)。结论高血压合并糖尿...     

Long-term cardiac effects of adrenalectomy or mineralocorticoid antagonists in patients with primary aldosteronism

Exposure to excess aldosterone results in cardiac damage in hypertensive states. We evaluated the long-term cardiac structural and functional evolution in patients with primary aldosteronism after surgical or medical treatment. Fifty-four patients with primary aldosteronism were enrolled in a prospective study and were followed for a mean of 6.4 years after treatment with adrenalectomy (n=24) or spironolactone (n=30). At baseline, echocardiographic measurements of patients with primary aldosteronism were compared with those of 274 patients with essential hypertension. Patients with primary aldosteronism had greater left ventricular mass, more prevalent left ventricular hypertrophy, lower early:late-wave diastolic filling velocities ratio, and longer deceleration time than patients with essential hypertension but no differences in relative wall thickness and systolic function. During follow-up, average blood pressure was 135/82 and 137/82 mm Hg in patients treated with adrenalectomy and spironolactone, respectively. In the initial 1-year period, left ventricular mass decreased significantly only in adrenalectomized patients. Subsequent changes in left ventricular mass were greater in patients treated with spironolactone, with an overall change from baseline to the end of follow-up that was comparable in the 2 groups. Prevalence of hypertrophy decreased in both treatment groups, whereas diastolic parameters had only mild and nonsignificant improvement. Changes in blood pressure and pretreatment plasma aldosterone were independent predictors of left ventricular mass decrease in both treatment groups. Thus, in the long-term, both adrenalectomy and spironolactone are effective in reducing left ventricular mass in patients with primary aldosteronism, with effects that are partially independent of blood pressure changes.     

Hochdruckherz und hypertensive Mikroangiopathie

Cardiac alterations in patients with arterial hypertension comprise the manifestation of stenosis in epicardial arteries, disease of coronary resistive vessels, prothrombotic changes and endothelial dysfunction, pronounced perivascular and interstitiell fibrosis, left ventricular hypertrophy, dilatation of the left atrium, increased sympathetic drive and degeneration of aortic valve. These alterations leads to the major clinical manifestations of hypertensive heart disease, that are symptoms of reduced coronary conductance, left ventricular hypertrophy, diastolic and systolic dysfunction with or without left ventricular enlargement and arrythmia. Different non-inavsive and invase procedures are available for screening and follow up of patients with hypertensive heart disease. The primary therapeutic target is, apart from lowering blood pressure, to reverse cardiac manifestations of arterial hypertension using specific therapeutic algorithms.     

Correlation between arterial pressure at rest and during effort and left ventricular mass in hypertensive patients who were never treated

A poor correlation has been found between blood pressure at rest and left ventricular mass in the course of several echocardiographic studies on hypertensive patients. The aim of this work was to determine if this finding could be the result of previous antihypertensive therapy, which had been suspended a few weeks previously in most of the studies. In addition, we tested whether blood pressure values during physical exercise correlate with the echocardiographic indices of left ventricular mass better than the values at rest. In our group of 43 patients with mild to moderate essential hypertension who had never been pharmacologically treated, the correlation between both systolic and diastolic blood pressure and left ventricular mass was poor (r = 0.41 and 0.30 respectively). This result suggests that one or more factors other than hypertension may determine the development of left ventricular hypertrophy. However, in 10 patients with left ventricular hypertrophy a more significant correlation was found between cardiac mass and diastolic pressure (r = 0.52), rather than systolic pressure (r = 0.33). This finding supports data indicating that cardiovascular risk is related more to diastolic pressure increments than to systolic pressure. As for blood pressure values during physical exercise, in our study they did not show a better predictivity of ventricular mass than the values at rest.