肥厚型心肌病患者60例心肌应变研究

目的探讨肥厚型心肌病(HCM)患者局部病变心肌的收缩特性。方法应用组织多普勒成像技术分析60例HCM患者及40例年龄及性别相匹配的正常对照者在心尖四腔切面6个心肌节段的收缩期最大应变。结果HCM组肥厚心肌收缩期最大应变显著低于对照组正常心肌[(-4.8±4.4)%vs(-19.7±4.0)%,P<0.001],区分HCM肥厚心肌与正常心肌的最佳截断点为-11.3%。结论HCM患者肥厚心肌收缩期纵向应变显著降低。心肌应变分析为识别肥厚型心肌病并定量评价其局部心肌收缩功能提供了新的方法。     

超声二维斑点追踪技术对陈旧性心肌梗死患者左室收缩同步性的定量研究

目的采用超声二维斑点追踪技术定量评价陈旧性心肌梗死患者左室收缩同步性。方法25例陈旧性心肌梗死患者和30例正常人为对照组,超声心动图观察其左心室短轴（二尖瓣、乳头肌、心尖）切面的二维灰阶动态图,二维斑点追踪分析软件获取各节段的径向应变、圆周应变、径向应变率和圆周应变率曲线,分别测量各节段从心电图QRS波起始至收缩期峰值径向应变、圆周应变、径向应变率、圆周应变率的时间及其标准时间：Trs、Tcs、Trsr、Tcsr、Trs—SD、Tcs—SD、Trsr—SD、Tcsr—SD。将心肌梗死组患者左室心肌分为梗死节段和非梗死节段,比较两组心肌间Trs、Tcs、Trsr、Tcsr的差异。结果心梗组患者Trs—SD、Tcs—SD、Trsr—SD、Tcsr—SD高于对照组（P〈0．05）,心肌梗死节段Trs、Tcs、Trsr、Tcsr较非心肌梗死节段延长（P〈0．05）。结论心肌梗死患者左室心肌存在收缩不同步运动,超声二维斑点追踪技术可以定量评价心肌梗死患者左室收缩同步性。     

定量组织速度成像、应变和应变率显像评价肥厚型心肌病与高血压心脏病左室心功能的对比研究

目的:探讨定量组织速度(QTVI)、应变(ε)和应变率(SR)显像在评价肥厚型心肌病(HCM)与高血压病患者局域心肌舒缩功能的临床应用价值。方法:比较肥厚型心肌病与原发性高血压病左室肥厚(LVH)患者不同心肌节段的定量组织速度、应变率值以及收缩期最大应变值。结果:HCM组Vs、Ve、SRs、SRe及ε测值均显著小于对照组且差异有显著性意义;HCM组部分心肌节段SRs、SRa、ε测值与高血压LVH组比较差异有显著性意义。结论:QTVI、ε和SR显像为评价肥厚型心肌病早期节段心肌功能异常及鉴别肥厚型心肌病与高血压性心肌肥厚提供了准确和实用的新方法。     

磁共振特征性追踪技术对肥厚型心肌病心肌应变的初步研究

目的采用心脏磁共振特征性追踪(cardiovascular magnetic resonance feature tracking,CMR-FT)技术对肥厚型心肌病患者的心功能及心肌节段应变进行分析,探讨CMR-FT对肥厚性心肌病患者早期运动异常检测的可行性。材料与方法对17例肥厚型心肌病患者及14名健康志愿者进行3.0 T SSFP电影序列扫描,使用CVI软件检测心功能,并对48个肥厚的心肌节段及健康志愿者中42个正常心肌节段进行特征性追踪(feature tracking,FT)后处理。结果肥厚型心肌病患者与健康志愿者左心功能参数(左心室舒张末期容积、左心室收缩末期容积及左心室射血分数)的差异无统计学意义(P均0.05),肥厚的心肌节段的圆周应变、长轴应变及峰值收缩期圆周应变、峰值收缩期长轴应变均低于正常的心肌节段[(-5.26±2.70)%vs(-11.68±2.06)%,(-7.92±5.07)%vs(-13.93±3.89)%,(-10.44±5.46)%vs(-18.43±2.99)%,(-12.29±8.17)%vs(-20.26±2.93)%,P均0.05]。结论对于心功能正常的肥厚性心肌病患者,CMR-FT技术能够早期检测出肥厚患者肥厚心肌节段应变的变化,提示心肌应变量的改变能够比左心室功能参数更早地发现心肌收缩功能异常。     

应变率显像对肥厚型心肌病心肌收缩和舒张功能的研究

目的　通过应变率显像评价肥厚型心肌病患者肥厚心肌的局部收缩和舒张功能。方法　10例肥厚型心肌病患者(HCM)与 20例正常对照者,获取左室室间隔长轴方向基底段、中段和心尖段的心肌应变率曲线,及中段肥厚的室间隔三层心肌的应变率曲线,测定应变率数值 (SR),包括收缩期峰值SR、舒张早期峰值SR和舒张晚期峰值SR,测量左室射血分数(EF)和二尖瓣口血流的E、A峰值。结果　HCM组肥厚节段心肌收缩期和舒张期的SR均低于正常组相应节段的测值(P<0. 05)。HCM组肥厚节段内层、中层及外层心肌收缩期和舒张期的SR均低于正常组对应节段各层的相应测值(P<0. 05)。HCM组肥厚节段各层心肌收缩期和舒张期SR之间的差异无显著性意义。两组间的EF和E/A值差异无显著性意义。结论　肥厚型心肌病肥厚心肌的SR明显降低,其各层之间SR的差异无显著性意义。     

三维斑点追踪成像评价肥厚型心肌病患者左心室整体和局部收缩功能

目的 应用三维斑点追踪成像(3D-STI)检测肥厚型心肌病(HCM)患者左心室心肌整体及各节段峰值应变, 评估HCM左心室收缩功能。方法 收集43例HCM患者(病例组)和23名健康志愿者(对照组), 病例组分为室间隔肥厚型HCM(sHCM)亚组(22例)、心尖肥厚型HCM(aHCM)亚组(8例)和混合型HCM(mHCM)亚组(13例), 对所有受检者进行3D-STI检测, 获得左心室射血分数(LVEF), 左心室心肌整体纵向峰值应变(GPLS)、圆周峰值应变(GPCS)、面积峰值应变(GPAS)、径向峰值应变(GPRS)及各节段峰值应变, 比较组间上述参数差异。结果 病例组LVEF与对照组比较无明显变化(P >0.05)。3D-STI中病例组与对照组比较左心室心肌GPLS、GPAS和GPRS均明显减低(P均 <0.01), GPCS无明显变化;心肌应变减低sHCM亚组主要集中于间隔基底段及中间段, aHCM亚组主要集中于心尖段, mHCM亚组主要集中于中间段及心尖段。结论 HCM患者左心室常规收缩功能参数可正常, 左心室心肌三维纵向应变、面积应变、径向应变减低, 可通过3D-STI进行检测, 不同类型HCM患者应变减低节段分布与肥厚部位有关。     

应变率成像评价肥厚型心肌病患者左室局部心肌舒张功能

目的 探讨应变率成像(strain rate imaging,SRI)技术评价肥厚型心肌病(hypertrophic cardiomyopathy,HCM)患者左室长轴方向局部心肌舒张功能的临床价值.方法 30例HCM患者和25例健康成人,在组织多普勒速度显像条件下,分别测量长轴方向上左心室不同心肌节段的收缩期峰值应变率(SRs)、舒张期快速充盈时相和心房收缩时相的峰值应变率(SRe和SRa)、等容舒张期峰值应变率(SRIVR),并计算SRIVR/SRs及SRe/SRa值.结果 与正常组比较,HCM患者各节段SRe、SRa、SRe/SRa均减低;HCM患者同一室壁不同节段间的SRe、SRe/SRa值存在不均质性,各参数在间隔和前壁肥厚的基底及中间段显著降低(P＜0.05),以室间隔中间段减低为甚.正常组左室壁心肌各节段SRIVR绝对值差异无统计学意义(P＞0.05),HCM患者的肥厚节段负向SRIVR绝对值显著大于无增厚节段和轻度增厚节段,肥厚节段平均SRIVR/SRs＞0.6.结论 应变率成像技术可敏感检测HCM患者左室长轴方向局部心肌舒张功能的异常改变,为临床从机械力学角度评价HCM患者心肌功能异常提供了新手段.     

磁共振心肌首过灌注成像评价肥厚型心肌病微循环功能障碍

目的 应用MR心肌首过灌注成像评价肥厚型心肌病患者局部心肌微循环障碍.方法 选取22例肥厚型心肌病患者(HCM组)和13名健康志愿者(对照组)行心脏MR (CMR)检查(包括左心室短轴电影、心肌首过灌注和延迟增强序列),测量左心室舒张末期各心肌节段心肌壁厚度、心肌信号强度最大上升斜率(Slopemax)和心肌延迟强化(DE).采用单因素方差分析比较对照组心肌节段、HCM组非肥厚性心肌节段亚组和肥厚性心肌节段亚组的Slopemaax以及不同肥厚程度心肌节段的SlopemaX,对有DE心肌节段和无DE心肌节段的Slopemax的差异采用独立样本t检验进行分析.结果 HCM组中非肥厚性心肌节段亚组和肥厚性心肌节段亚组Slopemax均明显低于对照组(P均<0.05),其中肥厚性心肌节段亚组的Slopemax较非肥厚性心肌节段亚组降低更为显著(P＜0.05);轻度肥厚心肌节段Sl0pemax高于中度、重度肥厚心肌节段(P均＜0.05),但中度与重度心肌肥厚节段Slopemax的差异无统计学意义(P＞0.05).DE心肌节段Slopemax明显低于无DE心肌节段(P＜0.05).结论 MR心肌首过灌注成像能可靠地检出HCM局部心肌的微血管功能障碍,为临床对HCM患者进行风险分层、制定治疗计划和预后评估提供有价值的信息.     

定量组织速度成像对肥厚型心肌病患者左心室局部收缩功能的研究

目的　应用定量组织速度成像 (QTVI)评价肥厚型心肌病 (HCM)患者左心室局部收缩功能。方法　应用QTVI离线分析 3 1例HCM患者和 2 0例正常对照者左室长轴和短轴方向各心肌节段的速度曲线 ,测量收缩期峰值速度 (Vs) ,计算左室后壁和室间隔各心肌节段在长轴与短轴方向速度的比值。结果　HCM组肥厚与非肥厚心肌节段的平均Vs降低 ,与对照组相比 ,绝大部分心肌节段差异有显著性意义 (P<0 .0 5) ,但HCM组肥厚与非肥厚心肌节段的平均Vs之间差异无显著性意义 (P >0 .0 5)。正常人长轴与短轴方向速度的比值均 >1,而HCM患者其比值明显降低 ,大部分比值 <1。结论　HCM患者尽管左室射血分数正常 ,但左室长轴方向各心肌节段收缩功能受损 ,损害不仅发生在肥厚的左室壁 ,非肥厚的室壁同样受到损害 ;QTVI能定量评价HCM患者左室局部收缩功能     

应变率成像评价肥厚型心肌病患者左心室局部功能和室壁运动同步性

目的 评价应变率成像技术在定量检测肥厚型心肌病(HCM)患者左心室局部心肌功能及室壁运动同步性中的价值.方法 HCM患者21例,根据室间隔及左室壁厚度分为3组:①非肥厚组(NH),室壁厚度≤11 mm,101节段;②轻度肥厚组(MH),11mm＜室壁厚度≤15 mm,86节段;③重度肥厚组,室壁厚度＞15mm,65节段.对照组18例,216节段.获取各受试者心尖四腔观、左室长轴及两腔观组织速度图像存盘供脱机分析.测量收缩期峰值应变率(SRs)、舒张早期峰值应变率(SRe)、舒张晚期峰值应变率(SRa),计算SRe/SRa;测量收缩期应变率达峰时间(TssR),并计算收缩期应变率达峰时间变异(CVTSSR);测量舒张早期应变率达峰时间(TESR),并计算舒张早期应变率达峰时间变异(CVTESR).结果 与对照组室壁节段比较,HCM组NH、MH、SH亚组SRs、SRe、SRe/SRa均显著降低,且三个亚组间SRe依次降低,即NH＞MH＞SH,NH与MH组间SRe/SRa差异无统计学意义,与NH、MH组比较,SH组SRe/SRa显著减低;与对照组比较,MH、SH组SRa显著降低,而NH组较对照组差异无统计学意义,且NH＞MH＞SH;与对照组比较,HCM组CVTSSR及CVTESR显著增大.结论 HCM患者无论有无室壁肥厚,其左室局部收缩舒张功能均受损;HCM患者左室心肌运动存在不同步现象,应变率成像技术能准确、定量评价其左室局部心肌功能及其左室心肌运动不同步.     

实时三维超声心动图评价左室心肌肥厚患者的心肌收缩同步性

目的应用实时三维超声心动图（RT3DE）检测左室心肌肥厚（LVH）对左室收缩同步性的影响。方法76例LVH患者分为肥厚型心肌病组（HCM组，34例）和高血压性心脏病组（HHD组，42例），RT3DE测量心率校正的16节段达收缩末最小容积的差值和标准差（Tmsv 16-Dif和Tmsv 16-SD）作为收缩同步性参数，并与对照组（Con组，40例）比较。结果HCM组的Tmsv 16-Dif和Tmsv 16-SD均显著高于HHD组和Con组，但HHD组和Con组之间无显著差异。结论LVH并不总是合并左室收缩不同步，HCM左室收缩同步性下降，而HHD左室同步收缩。RT3DE可同时检测左室16个节段的收缩同步性。     

二维应变参数评价扩张型心肌病患者左心室收缩同步性及其与心功能的关系

目的 探讨二维斑点追踪成像（2D-STI）应变参数评价扩张型心肌病（DCM）患者左心室收缩同步性的价值及其与心功能的关系。方法 收集DCM患者（DCM组）及对照组各25例,采用2D-STI技术获取左心室各节段纵向应变达峰时间、圆周应变达峰时间（Tls、Tcs）,分别计算左心室18节段纵向应变达峰时间标准差（Tls-SD）及最大差值（Tls-dif）,左心室心尖四腔心、三腔心、二腔心切面6节段纵向应变达峰时间标准差（Tls-SD-4、Tls-SD-3、Tls-SD-2）及最大差值（Tls-dif-4、Tls-dif-3、Tls-dif-2）,左心室18节段圆周应变达峰时间标准差（Tcs-SD）及最大差值（Tcs-dif）,左心室短轴二尖瓣、乳头肌、心尖水平6节段圆周应变达峰时间标准差（Tcs-SD-M、Tcs-SD-P、Tcs-SD-A）及最大差值（Tcs-dif-M、Tcs-dif-P、Tcs-dif-A）。结果 与对照组比较,DCM组整体及节段应变参数均显著增大（P均<0.05）;DCM组中,除Tcs-dif-P、Tcs-dif外,余应变参数均与左心室射血分数呈负相关（P均<0.05）;除Tcs-dif-M、Tcs-dif-P及Tcs-dif外,余应变参数均与舒张早期二尖瓣口峰值血流速度（E）/二尖瓣环运动速度（e）呈正相关（P均<0.05）。结论 DCM患者左心室整体及局部收缩期应变均存在不同步,收缩不同步可加剧心功能的恶化;2D-STI参数可以客观评价DCM患者左心室收缩不同步及其与心功能的关系。     

斑点追踪技术评价肥厚型心肌病左心室肌扭转运动

目的 应用斑点追踪技术研究肥厚型心肌病的左心室肌的旋转运动及扭转特征.方法 病例组为24例非对称性肥厚型心肌病患者,其中室间隔和左心室前、侧壁增厚归为病例组1,室间隔中上部肥厚归为病例组2;正常对照组为48名健康志愿者.采用GE Vivid 7超声诊断仪,采集左心室短轴二尖瓣水平、乳头肌水平、心尖水平二维图像,脱机分析得到不同水平、不同节段的旋转角度、旋转速度及扭转角度,计算舒张早期解旋率.结果 病例组乳头肌水平旋转角度较正常对照组趋向于逆时针方向,且病例组2与正常对照组差异有统计学意义(P<0.05);二尖瓣水平和心尖水平旋转运动三组间差异无统计学意义(P>0.05).病例组1、病例组2与正常对照组左心室舒张早期解旋率分别为(0.22±0.11)%/ms、(0.23±0.08)%/ms、(0.43±0.19)%/ms,病例组1和病例组2均较正常对照组降低(P<0.05).结论 肥厚型心肌病不同的表现型其左心室扭转及旋转运动表现不同;应用斑点追踪技术可以准确地评价肥厚型心肌病患者的左心室扭转及旋转运动.     

肥厚性心肌病心肌功能及收缩同步性斑点追踪显像评价

目的 应用斑点追踪显像技术(STI)评价射血分数(EF)正常的肥厚性心肌病(HCM)心肌应变及收缩同步性的变化情况,并探讨左室流出道梗阻对于上述指标的影响.方法 HCM组(n=34)和正常对照组(n=30)分别行超声心动图检查,根据静息状态下左心室流出道压差将HCM组分为梗阻型(n=15)和非梗阻型(n=19).采用STI技术测量患者径向(RS)、圆周方向(CS)、纵向(LS)、横向应变(TS)幅度以及左心室短轴乳头肌水平室间隔、左室后壁到达径向峰值应变的时间差值(SPWPSD).结果 HCM组与正常组相比EF值无明显差异,但各种应变均显著降低,SPWPSD升高.分组资料表明梗阻型患者较非梗阻型应变进一步降低,不同步性高于非梗阻型患者.结论 HCM早期即可出现心肌变形能力下降及收缩不同步,左心室流出道梗阻加剧上述变化.     

Impact of right ventricular dyssynchrony on left ventricular performance in patients with pulmonary hypertension

Pulmonary hypertension has been associated with right ventricular (RV) dyssynchrony which may induce left ventricular (LV) dysfunction and dyssynchrony through ventricular interdependence. The present study evaluated the influence of RV dyssynchrony on LV performance in patients with pulmonary hypertension. One hundred and seven patients with pulmonary hypertension (age 63 ± 14 years, systolic pulmonary arterial pressure 60 ± 19 mmHg) and LV ejection fraction (EF) >35 % were evaluated. Ventricular dyssynchrony was assessed with speckle tracking echocardiography and defined as the standard deviation of the time to peak longitudinal strain of six segments of the RV (RV-SD) and the LV (LV-SD) in the apical 4-chamber view. Mean RV-SD and LV-SD assessed with longitudinal strain speckle tracking echocardiography were 51 ± 28 and 47 ± 21 ms, respectively. The patient population was divided according to the median RV-SD value of 49 ms. Patients with RV-SD ≥49 ms had significantly worse NYHA functional class (2.7 ± 0.7 vs. 2.3 ± 0.7, p = 0.004), RV function (tricuspid annular plane systolic excursion: 16 ± 4 vs. 19 ± 4 mm, p < 0.001), LVEF (50 ± 10 vs. 55 ± 8 %, p = 0.001), and larger LV-SD (57 ± 18 vs. 36 ± 18 ms, p < 0.001). RV-SD significantly correlated with LV-SD (r = 0.55, p < 0.001) and LVEF (r = ?0.23, p = 0.02). Multiple linear regression analysis showed an independent association between RV-SD and LV-SD (β = 0.35, 95 %CI 0.21–0.49, p < 0.001). RV dyssynchrony is significantly associated with LV dyssynchrony and reduced LVEF in patients with pulmonary hypertension.     

Doppler tissue imaging: regional myocardial function in hypertrophic cardiomyopathy and in athlete's heart.

BACKGROUND: The distinction between hypertrophic cardiomyopathy (HCM) and the athlete's (AT) heart is an important clinical problem, and the analysis of regional myocardial function with Doppler tissue imaging may be useful in the differential diagnosis. OBJECTIVE: Our aim was to compare regional function assessed by Doppler tissue imaging in rowers and in a group of patients with HCM. METHODS: In 24 patients with nonobstructive HCM and in 20 competitive rowers with similar age, blood pressure, and heart rate, we analyzed with pulsed Doppler tissue imaging left ventricular (LV) regional function (velocities, time intervals, heterogeneity and asynchrony indices, and meridional gradient) in the longitudinal (8 segments, apical views) and in the radial (2 segments, short-axis view) axis. RESULTS: Compared with AT, patients with HCM showed: (1). systolic function; (a). longitudinal: lower velocities and meridional gradient; longer precontraction period (PCP); and higher PCP/LV contraction time; (b). radial: lower velocities and gradient; longer PCP; and higher PCP/LV contraction time; (2.diastolic function; (a). logitudinal: lower e (early diastolic), a (late diastolic), and e/a velocities; and longer prerelaxation time and time to peak e. The percentage of segments with e/a < 1 was 25% in the HCM group and 0% in the AT heart group; (b). radial: lower e velocity and gradient; lower e/a gradient; and longer medial prerelaxation and basal time to peak e. Most of these differences also occurred in the nonhypertrophied inferior wall of patients with HCM. CONCLUSIONS: There are significant differences between regional LV function of competitive rowers and patients with HCM. These differences (1). occur in systole and diastole; (2). affect velocities and time intervals; (3). are more striking in the long axis, but are also seen in the short axis, and (4). also occur in nonhypertrophied segments, suggesting the usefulness of the technique in the differential diagnosis between the 2 situations, namely in individuals that fall in Maron's "grey zone."     

Serial ultrasound evaluation of intramyocardial strain after reperfused myocardial infarction reveals that remote zone dyssynchrony develops in concert with left ventricular remodeling

This study noninvasively evaluated the development of left ventricular (LV) dyssynchrony following reperfused myocardial infarction (MI) in mice using an ultrasonic speckle-tracking method. Eight C57BL/6J mice were assessed by high-resolution echocardiography at baseline and at eight time-points following MI. Images were acquired at 1mm elevational intervals encompassing the entire LV to determine chamber volumes and radial strain. Receiver-operating characteristic (ROC) analysis of regional radial strain was used to segment the three-dimensional (3-D) LV into infarct, adjacent and remote zones. This in vivo segmentation was correlated to histologic infarct size (R = 0.89, p < 0.01) in a short-axis, slice-by-slice comparison. The onset of dyssynchrony during LV remodeling was assessed by standard deviation of time to peak radial strain in the infarct, adjacent and remote zones. It was discovered that the form of LV dyssynchrony that develops in the remote zone late after MI does so in concert with the progression of LV remodeling (R = 0.70, p < 0.05).     

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)