不同方法检测的高血压性左室肥厚预测复杂性室性心律失常的价值

为评价不同方法检测的高血压性左室肥厚预测复杂性室性心律失常的价值，本文用超声心动图、心电图、心脏ＸＸ光片三种方法研究了１１６例无并发症的轻、中度原发性高血压患者。结果表明：ＥＣＨＯ、ＥＣＧ、Ｘ—ｒａｙ对高血压性左室肥厚的检出率分别为３９．７％、２５．０％、２０．７％（ｐ＜０．０５）。复杂性室性心律失常在有无ＥＣＧ—ＬＶＨ、ｘ—ｒａｙ—ＬＶＨ组间无显著性差异（Ｐ＞０．０５），而在有无ＥＣＨＯ—ＬＶＨ组间差异显著（Ｐ＜０．０１）．ＥＣＨＯ—ＬＶＨ程度与复杂性室住心律失常的级别有较密切的关系（ｒ＝０．６１，Ｐ＜０．０１）。因此认为，ＥＣＨＯ重量指数法检测的ＬＶＨ不仅是判断ＬＶＨ的可靠指标，而且对预测复杂性室性心律失常有重要价值。     

多普勒超声对依那普利逆转高血压左室肥厚的评价

作者应用转换酶抑制剂（ＡＣＥＩ）──依那普利（Ｅｎａｌａｐｒｉｌ）对３０例轻、中度高血压病患者进行治疗。观察８周后发现：①该药能有效控制血压，治疗前后比较收缩压、舒张压均明显下降（Ｐ＜０．００１），而并无心率增快的副作用；②能逆转左室肥厚（ＬＶＨ），减轻左室心肌重量、左室心肌重量指数等指标（Ｐ＜０．００１）；③对左室收缩功能指标如射血分数等没有明显影响（Ｐ＞０．００５）；④能改善左室舒张功能指标，而以ＰＥ／ＰＡ、Ｅｉ／Ａｉ最为显著Ｐ＜０．００１。结果提示，应用依那普利治疗高血压，短时间内（８周）不仅能有效控制血压，且具有一定逆转ＬＶＨ和改善左室舒张功能的作用。     

内皮素与高血压及左室肥厚的关系

目的：探讨高血压病患者血浆内皮素（ＥＴ）变化及与左室肥厚的关系。方法：６５例高血压患者伴左室肥厚３０例,无左室肥厚３５例,３０例正常人接爱放免法内皮素含量测定,超声心动图检查计算左室重量指数,分为ＬＶＨ经及ＮＬＶＨ组。结果：高血压病患者血浆内皮素明显高于正常人（Ｐ〈０．０１）,ＬＶＨ组较ＮＬＶＨ组为高（Ｐ〈０．０１）,ＥＴ含量与ＬＶＭＩ呈正相关（ｒ＝０．７１,Ｐ〈０．０５）。结论：血管内皮产生的Ｅ     

高血压病左室肥厚的动态血压与彩色多普勒关系的研究

本文对２００例高血压患者进行了２４小时动态血压监测（ＡＰＢＭ），并且全部病例进行了彩色多普勒超声检查。根据心肌重量（ＬＶＭ）和心肌重量指数（ＬＶＭＩ），将左室壁分为有无肥厚两组。结果发现：夜间平均收缩压和平均舒张压下降率与ＬＶＭ和ＬＶＭＩ呈显著负相关。更进一步研究说明，血压昼夜节律消失的高血压患者，左室肥厚检出率为４３％。左室肥厚者血液动力学改变Ｅ峰减低，Ａ峰明显增高，Ｅ峰减速度（ＥＤＣ）减小，检出率８１．９％高于非左室肥厚者，Ｐ＜０．００１。收缩功能与ＬＶＭ、ＬＶＭＩ呈显著负相关。表明高血压患者夜间血压水平与血压昼夜节律状况对左室肥厚发生和发展起主导作用，而左室肥厚的有无又与彩色多普勒超声的血液动力学改变具有密切关系。     

不同方法检测的高血压性左室肥厚预测复杂性心律失常的价值

为评价不同方法检测的高血压性左室肥厚测复杂性室性心律失常的价值，本文用超声心动图、心电图、心脏Ｘ光片三种方法研究了１１６例无并发症的轻、中度原发性高血压患者。结果表明：ＥＣＨＯ、ＥＣＧ、Ｘ－ｒａｙ对高血压性左室肥厚的检出率分别为３９．７％、２５．０％、２０．７％（Ｐ＜０．０５）。复杂性室性心律失常在有无ＥＣＧ－ＬＶＨ、ｘ－ｒａｙ－ＬＶＨ组间无显著怀差异，而在有无ＥＣＨＯ－ＬＶＨ组间差异显著（Ｐ＜０     

苯那普利伍用美托洛尔对高血压病左室舒张功能的影响

目的：采用转换酶抑制剂合用β－ 受体阻滞剂治疗高血压病, 旨在探讨两者对肥厚心肌及舒张功能的影响。方法：符合ＷＨＯ／ＩＳＨ高血压病Ⅰ、Ⅱ期病人,停用降压药两周,记录基础血压、心率,加用苯那普利及美托洛尔, 血压采用Ｋｏｒｏｔｋｏｆｆ 法测清晨血压, 采用超声心动仪, 分别测量ＬＶＩＤｄ、ＬＶＰＷＴｄ、ＩＶＳＴｄ、ＥＦ、Ａ峰、Ｅ峰、Ａ／Ｅ。并计算ＬＶＭＩ,治疗２４ 周后重复上述检查。结果：ＬＶＩＤｄ、ＬＶＰＷＴｄ、ＩＶＳＴｄ、ＬＶＭＩＴ等有不同程度下降, 左室舒张功能有不同程度改善（Ｐ均＜ ０．０１）。结论：两者合用,可有效抑制ＡｎｇＩＩ,逆转肥厚左室心肌, 改善左室舒张功能, 提高患者生活质量。     

高血压病患者血浆心钠素与左房血流动力学变化的关系研究

应用超声心动图技术和放射性免疫测定法对１００例高血压病患者左房血流动力学变化与血浆心钠素水平的关系进行分析研究。结果示：高血压左室肥厚组和非左室肥厚组血浆心钠素水平显著高于正常对照组（Ｐ＜０．００１）；且左室肥厚组与非左室肥厚组之间亦有显著性差异。血浆心钠素水平与左房功能指标ＬＡＶ、ＬＡＴ、ＬＡＰ、ＬＡＦ及ＭＡＰ呈高度线性相关；与ＬＡＤ、ＬＶＭＩ、ＬＶＥＦ、ＰＦＲ、Ａ峰、ＬＶＤ、Ａ／Ｅ呈中度相关（相关系数依次为：０．８１、０．８０、０．７８、０．７６、０．７０、０．６８，－０．６１、０．６０、０．６７、０．５０及０．４８，Ｐ＜０．０１～０．００１），但与Ｅ峰不相关（ｒ＝０．１６，Ｐ＞０．０５）。随着高血压病程及分期的增加，血浆心钠素水平有增加趋势。结论认为定量测定血浆心钠素将有助于评价高血压病患者左房血流动力学及左室功能的异常变化程度。     

超声检测高血压病患者左室心肌重量指数与心律失常关系的探讨

本文将我院７３例高血压病患者行彩色多普勒超声心动图检查所得各项心脏参数，按ＤｅｖｅｒｅｕｘＲＢ推荐的公式计算出左室心肌重量指数ＬＶＭＩ（ｇ／ｍ￣２）＝０．８｛１．０４（ＬＶＩＤｄ＋ＩＶＳＴｄ＋ＰＷＴｄ）￣３－（ＬＶＩＤｄ）￣３｝＋０．６，分成两组：重度心肌增重组ＬｖＭＩ男≥１２５ｇ／ｍ￣２，女≥１２０ｇ／ｍ￣２；轻度心肌增重组ＬＶＭＩ男１１０～１２５ｇ／ｍ￣２，女９０～１２０ｇ／ｍ￣２，同时监测各例患者２４小时动态心电图。结果表明：重度心肌增重组心律失常的发生率明显高于轻度组。将心律失常分为室性、室上性及传导阻滞三种类型，各型相比：重度组室性心律失常发生率高于轻度组。因而我们认为左室心肌重量指数与心律失常的发生呈正相关，这对高血压病患者预测病情及防治具有重要意义。     

高血压病心失常监测及治疗观察

本文对１１０例高血压病合并左室肥厚及８９例高血压而无左室肥厚者进行了动态心图监测，结果表明高血压病合并左室肥厚者，其室性心律失常、其它心律失常及复合性心律失常的产生平均高于非左室肥厚组，两者对比存在非常显著性差异（Ｐ〈０．０１）。本组左室肥厚（ＬＶＨ）组律失常的发生率大大增高。因此提示临床医生应高度警惕左室肥厚的危害。     

心肌肥厚对冠脉循环影响的超声研究

目的： 探讨心肌肥厚患者冠脉循环血流动力学变化的特点。方法： 应用多平面经食管超声心动图（ＴＥＥ） 技术探测３０ 例心肌肥厚患者的冠状窦血流动力学改变, 并与１０ 例正常对照进行对比。结果： 所有受检者均可记录到满意的冠状窦血流频谱 （１００％ ）。心肌肥厚组收缩压、左室重量指数 （ＬＶＭ Ｉ）、冠状窦收缩期血流流速积分 （ＶＴＩ－Ｓ）、净前向血流流速积分 （ＶＴＩｎｅｔ） 和前向血流 （ＣＳＦ） 及其直径明显高于正常组 （Ｐ 均＜ ０．０５）, 余各项参数无显著性差异; 与正常组相比, 心肌肥厚患者有症状组收缩压、舒张压、ＬＶＭ Ｉ、ＶＴＩｎｅｔ 及冠状窦直径明显增加 （Ｐ＜ ０．０５～０．００１）; 无症状组ＬＶＭ Ｉ、收缩压、舒张期血流峰值 （Ｄ）、ＶＴＩ－Ｓ、舒张期血流流速积分 （ＶＴＩ－Ｄ）、ＶＴＩｎｅｔ、ＣＳＦ 亦明显增加 （Ｐ＜ ０．０５～０．００１）; 但有症状组Ｄ、ＶＴＩ－Ｄ、ＣＳＦ 低于无症状组 （Ｐ 均＜ ０．０５）。结论： 心肌肥厚患者冠状窦前向血流增加, 但有症状组冠状窦前向血流低于无症状组, ＴＥＥ 探测冠状窦血流以评价心肌肥厚患者冠脉循环的改变具有较高的临床应用价值。     

超声心动图四维自动左心室容积测定技术在左心室室壁瘤成形术中的应用价值

目的 探讨四维自动左心室容积测定（4D auto LVQ）在室壁瘤左心室成形术中的应用价值。方法 采用4D auto LVQ技术评价7例广泛前壁心肌梗死合并心尖部室壁瘤患者左心室容积和功能,并与心脏MR测量心室容积及室壁瘤成形术后左心室收缩功能比较。结果 5例术前行心脏MR检查,5例行室壁瘤成形术。与二维超声心动图相比,4D auto LVQ测量室壁瘤患者左心室容积与心脏MR检查结果更接近。采用4D auto LVQ技术术前预测左心室收缩功能与术后实际左心室收缩功能接近。结论 4D auto LVQ技术可更精准、快捷地评价左心室容积和收缩功能,为制定室壁瘤成形手术方案提供客观资料。     

New strategies for ventricular tachycardia and ventricular fibrillation ablation

Patients with ventricular tachycardia (VT) and ventricular fibrillation (VF) and no reversible cause are difficult to treat. While implantable defibrillators prolong survival, many patients remain symptomatic due to device shocks and syncope. To address this, there have been recent advances in the catheter ablation of VT and VF. For example, non-invasive imaging has improved arrhythmia substrate characterisation, 3D catheter navigation tools have facilitated mapping of arrhythmia and substrate and ablation catheters have advanced in their ability to deliver effective lesions. However, the long-term success rates of ablation for VT and VF remain modest, with nearly half of treated patients developing recurrence within 2–3 years, and this drives the ongoing innovation in the field. This review focuses on the challenges particular to ablation of life-threatening ventricular arrhythmia, and the strategies that have been recently developed to improve procedural efficacy. Patient sub-groups that illustrate the use of new strategies are described.     

室性心动过速和心室颤动治疗进展

室性心动过速（室速）和心室颤动（室颤）是心源性猝死最常见的原因。本文就器质性、特发性和离子通道病性室速/室颤的药物、器械、导管消融术及其他治疗等的最新进展进行了总结,以期能够达到规范临床诊疗的作用。     

室性早搏对左心室功能的影响

室性早搏是临床上最常见的心律失常,本文综述了室性早搏的形态、起源、负荷等特点对左心室功能的影响。室性早搏负荷大于20%,QRS时限>150 ms以及右心室起源的室性早搏更容易伴随或导致左心室功能下降。临床上对于频发室性早搏的及时治疗,能够起到改善心功能或预防心功能恶化的目的。导管射频消融治疗已成为特发性室性心律失常的最有效的治疗方法。     

Left ventricular hypertrophy, compliance and ventricular filling.

A total of 20 untreated hypertensive patients were divided into two equal groups matched for sex, age and blood pressure but with [mean diastolic wall thickness (MDWT) greater than 1.2 cm] or without (MDWT greater than 1.2 cm) left ventricular hypertrophy (LVH). All patients underwent pulsed doppler echocardiography and 99Tc radionuclide ventriculography at rest to assess diastolic and systolic abnormalities. In hypertensives with LVH the interventricular wall thickness, posterior wall thickness and relative diastolic wall thickness were significantly (P less than 0.01) higher and peak filling rate was significantly (P less than 0.01) lower than in hypertensives without LVH. The indices of systolic function, however, were not significantly different in the two patient groups. In hypertensives without LVH peak filling rate directly correlated with heart rate, whereas in those with LVH peak filling rate directly correlated with heart rate and the ratio of peak velocity of early left ventricular filling : peak velocity of late left ventricular filling due to atrial contraction. It is concluded that diastolic parameters may be useful tools for assessing myocardial compliance and may be effective markers of diastolic dysfunction.     

Effect of pacing-induced ventricular dyssynchrony on right ventricular function

Background: Asynchronous electrical activation induced by right ventricular (RV) pacing can cause several abnormalities in left ventricular (LV) function. However, the effect of ventricular pacing on RV function has not been well established. We evaluated RV function in patients undergoing long‐term RV pacing. Methods: Eighty‐five patients and 24 healthy controls were included. After pacemaker implantation, conventional echocardiography and strain imaging were used to analyze RV function. Strain imaging measurements included peak systolic strain and strain rate. LV function and ventricular dyssynchrony by tissue Doppler imaging (TDI) were assessed. Intra‐ and interobserver variabilities of TDI parameters were tested on 15 randomly selected cases. Results: All patients were in New York Heart Association functional class I or II and percentage of ventricular pacing was 96 ± 4%. RV apical induced interventricular dyssynchrony in 49 patients (60%). LV dyssynchrony was found in 51 patients (60%), when the parameter examined was the standard deviation of the time to peak myocardial systolic velocity of all 12 segments greater than 34 ms. Likewise, septal‐to‐lateral delay ≥65 ms was found in 31 patients (36%). All echocardiographic indexes of RV function were similar between patients and controls (strain: ?22.8 ± 5.8% vs ?22.1 ± 5.6%, P = 0.630; strain rate: ?1.47 ± 0.91 s^?1 vs ?1.42 ± 0.39 s^?1, P = 0.702). Intra‐ and interobserver variability for RV strain was 3.1% and 5.3%, and strain rate was 1.3% and 2.1%, respectively. Conclusions: In patients with standard pacing indications, RV apical pacing did not seem to affect RV systolic function, despite induction of electromechanical dyssynchrony. (PACE 2011; 34:155–162)