原发性醛固酮增多症患者与左心室肥厚

目的探讨原发性醛固酮增多症（原醛）及其主要亚型：腺瘤型和增生型的左室肥厚情况。方法入选确诊原醛患者250例。其中142例行分侧肾上腺静脉取血，分为原醛腺瘤组68例，原醛增生组74例，选取同期年龄、性别、24小时平均血压相匹配的原发性高血压（EH）患者246例作为对照，所有入选者记录一般临床资料和生化指标，并行超声心动图检查。结果1）左室舒张末期内径原醛组[（49．6±4．3）mm]高于EH组[（48．3±4．2）mm，P〈0．053，原醛组左室后壁厚度[原醛组（10．5±2．2）mm vs EH组（9．9±1．1）mm]、左室质量（LVM）[原醛组（232．2±75．1）g vs EH组（207．5±46．6）g]、左室质量指数（LVMI）[原醛组（131．9±37．4）g／m^2 vs EH组（118．3±23．7）g／m^2]显著高于EH组（P均〈0．01）。2）在原醛组中LVMI与收缩压及立位血浆醛固酮独立相关。3）1级高血压中原醛组的LVMI高于EH组，但差异无统计学意义（P〉0．05）；2级、3级高血压中，原醛组的LVMI高于EH组（P〈0．05或P〈0．01）。4）左室后壁厚度[原醛组（10．8±3．0）gVSEH组（10．3±1．3）g，P〈0．053；、LVM[原醛组（249．5±81．7）g vs EH组（219．4±67．7）g，P〈0．01]、LVMI[原醛组（139．9±41．0）g／m^2 vs EH组（125．1±32．9），P〈0．01]原醛腺瘤组显著高于原醛增生组。5）左室肥厚在EH组、原醛腺瘤组和增生组的构成比分别为42．7％，63．2％和43．2％，3组之间差异有统计学意义（P=0．009）。结论原醛患者左室肥厚的发病率高于EH患者，其中以原醛腺瘤组更为严重。     

原发性醛固酮增多症患者左室结构损害的研究

目的 探讨原发性醛固酮增多症(PA)患者左室结构损害的特点.方法 将2007年1月至2010年6月住院行PA筛查最终确诊为PA(213例)及原发性高血压(EH)的患者(225例)纳入研究,依据超声心动图结果评价两组患者的左室结构.结果 PA组的病程、醛固酮水平明显高于EH组(P＜0.01),而血钾、肾素活性明显低于EH组(P＜0.01).协方差分析校正病程后,PA组患者的室间隔厚度、左室舒张末期内径、左室重量指数、左室舒张末期容积和每搏输出量均高于EH组(P＜0.01).PA组患者左室肥厚的发生率明显高于EH组(53.1％对33.8％,x2=16.57,P＜0.01);PA组患者正常构型、向心性重构、向心性肥厚及离心性肥厚的构成比分别是:24.9％、22.1％、22.1％和30.9％.多元逐步回归分析显示收缩压、坐位醛固酮水平是影响PA患者左室重量指数的主要因素,回归系数分别为0.45 (P＜0.01)、0.43 (P＜0.01);病程是影响相对室壁厚度的主要因素,回归系数是0.011 (P＜0.05).结论 PA患者左室肥厚的发生率高于EH患者,其左室构型以离心性肥厚最多见.     

原发性醛固酮增多症左心室肥厚及相关影响因素分析

目的探讨原发性醛固酮增多症（原醛）患者的并发症情况,分析原醛患者左心室肥厚的相关因素。方法对93例原发性醛固酮增多症（原醛组）患者及同期住院的84例原发性高血压（原高组）患者的临床资料进行回顾性分析。结果（1）与原高组患者相比,原醛组患者血钙水平更低（P〈0．05）,但脂代谢异常程度较轻。（2）原醛组患者左心室肥厚较原高组患者严重,相关分析显示,原醛组患者的左心室质量与低血钾病程（r=0．983,P〈0．01）、立位醛固酮水平（r=0．993,P〈0．01）呈显著正相关,而与血钾（r=-0．993,P〈0．01）呈显著负相关。结论原醛组患者与原高组患者相比血钙水平更低,左心室肥厚更严重,但脂代谢异常程度较轻;原醛组患者的左心室质量与低血钾病程、立位醛固酮水平和血钾水平具有相关性。     

原发性醛固酮增多症

原发性醛固酮增多症(原醛症)是继发性高血压的常见病因之一,部分患者亦可伴有低血钾,醛固酮瘤及特发性醛固酮增多症是其主要的病理亚型。原醛症的诊断包括筛查、确诊及分型诊断3个步骤,传统影像学结合体位刺激的方法进行分型诊断,假阳性及假阴性率均较高,肾上腺静脉插管采血可作为影像学检查的补充。醛固酮瘤及原发性肾上腺增生患者应予手术治疗,特发性醛固酮增多症患者多采用药物治疗,螺内酯是其首选药物。     

原发性醛固酮增多症的诊疗进展

1955年Conn首次描述了以高血压、低钾血症、低肾素活性和高醛固酮分泌为特点的原发性醛固酮增多症(PA)。过去观点认为原发性醛固酮增多症仅占高血压患者中的0．4％～2％,并且对其认识不足,因而未引起足够的重视,从而使大量的原发性醛固酮增多症患者未得到正确的诊断和合理的治疗。本文将从原发性醛固酮增多症的筛查、诊断以及治疗等方面观点的更新作一综述。     

原发性醛固酮增多症的肾脏损害

原发性醛固酮增多症（Primary Aldosteronism,原醛）近十余年由于诊断方法的改进,由过去占高血压发病率大约1％上升到10％,在难治性高血压中更高达17～23％,成为目前最常见的继发性高血压。已证实醛固酮为独立于血压水平的心血管危险因素,更是肾脏中、小动脉受损及肾病的独立危险因素。一项6．4年随访原醛患者的肾脏功能损害情况,发现原醛患者的肾脏功能损害较原发性高血压（Primary Hypertension,原发性高血压）患者更严重。本文就原醛的醛固酮引起肾脏损伤机制做一综述。     

原发性醛固酮增多症患者糖代谢紊乱情况分析

目的 探讨原发性醛固酮增多症（原醛）患者糖代谢紊乱的发生率及其临床特征.方法 分析2008-10-2010-07我院确诊的原醛患者的临床资料并进行统计分析,分析原醛患者中糖代谢紊乱的患病情况,分别根据性别、年龄、民族、体质量指数(BMI)、高血压病程及醛固酮水平进行分组,其中男性患者115例、女性患者98例.比较不...     

原发性醛固酮增多症的分型诊断

目的 探讨用于原发性醛固酮增多症(原醛症)分型诊断检查方法的价值.方法 收集本院近7年来57例临床确诊的原醛症患者[醛固酮瘤22例,特发性醛固酮增多症(特醛症)26例,原发性肾上腺增生9例],检测患者的血电解质、血浆肾素活性及血、尿醛固酮,将结果与19例原发性高血压患者对照.再通过肾上腺CT、体位激发试验及肾上腺静脉采血检查对原醛症患者分型并随访.结果 (1)醛固酮瘤患者血压及血、尿醛固酮较特醛症患者高,血钾及血浆肾素活性则低,而原发性肾上腺增生患者临床及生化改变介于两者之间.肾上腺CT检查在原醛症分型诊断中的符合率为醛固酮瘤86.4%,特醛症73.1%,原发性肾上腺增生22.2%;肾上腺静脉采血检查以两侧醛固酮之比作为判定标准时符合率为86.4%、80.8%和77.8%,以醛固酮与皮质醇之比为判定标准则符合率分别为95.5%、92.3%及100.0%.(2)醛固酮瘤及原发性肾上腺增生患者术后随访血醛固酮均下降,血压恢复正常者分别为22.7%及44.9%,血钾恢复正常者为83.3%及100.0%,而特醛症患者随访中各项测值无明显变化,另有33.3%诊断时血钾正常的患者随访中出现低血钾.结论 原醛症的分型诊断需依靠多种检查手段综合分析,单纯依赖影像学检查或体位激发试验并不可靠,肾上腺静脉采血检查可作为影像学检查的补充,用两侧醛固酮与皮质醇的比值分析较单纯比较两侧醛固酮之比更为可靠;醛固酮瘤及原发性肾上腺增生患者术后临床及生化测值均得以明显改善,而特醛症患者随访中无明显变化.     

原发性醛固酮增多症患病率的争论

原发性醛固酮增多症在高血压人群中患病率的争论持续存在,已成为临床关注的焦点。现基于近年来国内外对原发性醛固酮增多症患病率的研究,分析原发性醛固酮增多症患病率争论的原因,探讨原发性醛固酮增多症筛查、诊断中存在的问题,提出解决问题的建议。     

Left Ventricular Hypertrophy in Patients with X-Linked Hypophosphataemia

X-linked hypophosphatemia (XLH) is a rare genetic disorder with X-linked dominant inheritance. Mutations in the PHEX gene increase fibroblast growth factor 23 (FGF23) concentrations, causing loss of phosphorus at the proximal tubule. Most pediatric patients debut in the first two years with short stature and bowed legs. Conventional treatment consists of oral supplements with phosphorus and calcitriol. Since 2018, burosumab has been approved as a novel therapeutic option for XLH, with promising results. The purpose of this study was to share our experience with two cases of XLH treated with burosumab. These patients presented with a broad phenotypical differences. One had the most severe radiological phenotype and developed left ventricular hypertrophy (LVH) and left ventricular dysfunction with preserved ejection fraction. Treatment with burosumab was well-tolerated and was followed by radiological stability and a striking improvement in both blood biochemistry and quality of life. The LVH was stable and left ventricular function normalized in the patient with cardiac involvement. In recent years many studies have been carried out to explain the role of FGF23 in cardiovascular damage, but the exact pathophysiological mechanisms are as yet unclear. The most intensively studied populations are patients with XLH or chronic kidney disease, as both are associated with high levels of FGF23. To date, cardiovascular involvement in XLH has been described in patients treated with conventional treatment, so it would be of interest to investigate if early use of burosumab at the time of diagnosis of XLH would prevent the occurrence of cardiovascular manifestations.     

单纯收缩期高血压患者左心室肥厚与室性心律失常的关系

目的探讨单纯收缩期高血压的病人左室肥厚与心律失常的关系。方法采用２４ｈ动态心电图和彩色多普勒超声观察患者左室肥厚及心律失常的发生情况，并观察单纯收缩期高血压与舒张期高血压左室结构改变。结果左室肥厚组室性心律失常发生率明显高于非左室肥厚组（Ｐ＞０．０１），单纯收缩期高血压组左室肥厚高于舒张期高血压组。结论左室肥厚可使室性心律失常发生率增加，收缩压增高较舒张压增高更易导致左室肥厚。     

高血压左室肥厚病人的肾功能评价

目的研究高血压伴左室肥厚患者肾功能的改变。方法对３０例高血压伴左室肥厚病人及２１例年龄相当的健康人对照组行核素动态肾功能检测及彩色多普勒超声肾血流动力学检查,测定肾小球滤过率（ＧＦＲ）和肾脏指数（ＲＩ）及肾内动脉分布,段动脉、叶间动脉的阻力指数（ｒｉ）,血流峰速加速时间（ＡＴ）,收缩期最大血流速度（ＶＳ）,舒张期末最低血流速度（ＶＤ）。结果观察组肾内弓形动脉、小叶间动脉较对照组明显减少甚至不能显示,肾内段动脉和叶间动脉的阻力指数（ｒｉ）显著增加（Ｐ＜０．００１）,ＡＴ明显延长（Ｐ＜０．００１）,ＧＦＲ显著降低（Ｐ＜０．００１）,ＶＳ,ＶＤ及肾脏指数（ＲＩ）亦明显降低（Ｐ＜０．０１）。结论当临床血肌酐、尿素氮均正常时,高血压病伴左室肥厚的很多患者已经有肾功能的改变,早期检测和发现这种肾脏功能的改变有助于阻止高血压的进展和指导治疗     

Electrocardiographic Criteria of Left Ventricular Hypertrophy in Patients with Morbid Obesity

Background: Obesity is frequently accompanied by systemic hypertension complicated by left ventricular hypertrophy (LVH). Standard electrocardiography (ECG) is generally accepted screening tool for LVH in systemic hypertension. The aim was to assess currently used ECG criteria in the diagnosis of LVH in morbidly obese patients. Methods: Ninety‐five patients (80 women, 15 men) with body mass index ≥ 40 kg/m², prior to scheduled bariatric surgery were included into the study. All patients underwent standard ECG and transthoracic ECG for LVH assessment. Results: Echocardiographically LVH (>110 g/m² in women, and >132 g/m² in men) was diagnosed in 54 patients (56.8%). None of the ECG criteria showed satisfactory performance in the diagnosing echocardiographically confirmed LVH. Although, Receiving operating curves (ROC) analysis showed that only Romilht‐Estes score and Cornell index × QRS complex duration were characterized by area under curve >0.6 (0.662; 0.612, respectively),currently recommended values of both tests (Romilht‐Estes score and Cornell index × QRS duration 2436 mm · ms) showed very low sensitivity in morbidly obese patients (0% and 2%, respectively). Conclusions: Our study showed that none of voltage‐based ECG criteria are of value for LVH diagnosis in severely obese patients. Only Romhilt‐Estes scale and Cornell indices could be helpful for the identification of LVH in the group of patients with morbid obesity, but their value is far from being satisfactory. Ann Noninvasive Electrocardiol 2011;16(3):258–262     

依那普利对高血压左室肥厚的逆转效应

本文对依那普利治疗原发性高血压时的左室肥厚逆转效应进行观察。根据心超LVMI分为肥厚组 (2 4例 )和非肥厚组 (13例 )。疗程 4周 ,剂量 10～ 40mg/d。结果显示左室肥厚的逆转效应在短期 (4周 )治疗后可出现 ,首先是IVST的下降。对左室无肥厚者起相反效应     

The Effects of Simvastatin on Left Ventricular Hypertrophy and Left Ventricular Function in Patients with Essential Hypertension

This study is to evaluate the effects of Simvastatin on left ventricular hypertrophy and left ventricular function in patients with essential hypertension. Untreated or noncompliance with drug treatment patients with simple essential hypertension were treated with a therapy on the basis of using Telmisartan to decrease blood pressure (BP). There were 237 patients who had essential hypertension combined with left ventricular hypertrophy as diagnosed by echocardiography, taken after their BPs were decreased to meet the values of the standard normal. Among them, there were only 41 out of the original 237 patients, 17.3%, who had simple essential hypertension combined with left ventricular hypertrophy without any other co-existing disease. They were the patients selected for this study. All patients were randomly, indiscriminately divided into two groups: one was the control group (Group T), treated with the Telmisartan-based monotherapy; the other was the target group (Group TS), treated with the Telmisartan-based plus simvastatin therapy. The changes of left ventricular hypertrophy and left ventricular function were rediagnosed by echocardiography after 1 year. The results we obtained from this study were as follows: (i) The average BPs at the beginning of the study, of simple essential hypertension combined with left ventricular hypertrophy, were high levels (systolic blood pressure (SBP) 189.21 ± 19.91 mm Hg, diastolic blood pressure 101.40 ± 16.92 mm Hg). (ii) The Telmisartan-based plus simvastatin therapy was significantly effective in lowering the SBP (128.26 ± 9.33 mm Hg vs. 139.22 ± 16.34 mm Hg). (iii) After the 1-year treatment, the parameters of left ventricular hypertrophy in both groups were improved. Compared to group T, there were no differences in the characteristics of the subjects, including interventricular septum, left ventricular mass, left ventricular mass index, ejection fraction, left atrium inner diameter at baseline. The patients’ interventricular septum (Group TS 10.30 ± 1.80 mm vs. Group T 10.99 ± 1.68 mm, P < .05), LVM (Group TS 177.43 ± 65.40 g vs. Group T 181.28 ± 65.09 g, P < .05), and LVMI (Group TS 100.97 ± 37.33 g/m² vs. Group T 106.54 ± 27.95 g/m², P < .05), all dropped more prominently (P < .05) in group TS; the ejection fraction rose more remarkably in group TS (Group TS: 57.50 ± 16.41% to 65.43 ± 11.60%, P < .01 while showing no change in Group T); the left ventricular hypertrophy reversed more significantly and the left ventricular systolic function improved more. (iv) The left atrium inner diameter of Group TS decreased (P < .01), the ratio of E/A, which indicates the left ventricular diastolic function, continued to drop further, showing no change to the trend of left ventricular diastolic function declination. Patients who have hypertension with left ventricular hypertrophy usually suffer other accompanying diseases at the same time. Telmisartan-based plus Simvastatin treatment can significantly reduce SBP, reverse left ventricular hypertrophy, improve the left ventricular systolic function, but it has no effect on reversing the left ventricular diastolic function. This experiment indicated that Simvastatin can reverse left ventricular hypertrophy and improve left systolic function.     

高血压左室肥厚与室性心律失常的研究进展

研究表明高血压左室肥厚的患者室性心律失常,尤其是复杂性室性心律失常发生率增高,目前认为主要与左室重构、心肌缺血、肥厚心肌的电生理改变、神经内分泌因子分泌异常等多种因素有关。在对高血压病的患者进行降压治疗的同时逆转左室肥厚能减少室性心律失常的发生,肾素-血管紧张素系统抑制剂因在此方面作用显著而倍受关注。