原发性高血压患者心肌能量消耗水平变化与左心室舒张功能的关系

目的探讨左心室舒张功能障碍与舒张功能正常的原发性高血压患者心肌能量消耗(MEE)水平的不同及其临床意义。方法选取原发性高血压患者128例,分别用组织多普勒和脉冲多普勒成像技术测量左心室舒张功能指标二尖瓣环舒张早期及舒张晚期运动速度之比(E'/A')、二尖瓣口舒张早期及舒张晚期血流速度之比(E/A)以及F/F';同时测量心脏结构指标、收缩功能指标,计算左心室收缩末周向室壁应力(cESS)、MEE。根据E'/A'将患者分为Gl组(E'/A'≥1)和G2组(E'/A'<1),根据E/A分为G3组(E/A≥1)和G4组(E/A<1),根据E/E'分为G5组(E/E'≥8)和G6组(E/E'<8)。结果 G2组左心房内径、左心室内径、室间隔厚度、左心室后壁(PWTd)、左心室质量指数、cESS及MEE明显高于G1组,LVEF明显低于G1组(P<0.01);G4组年龄、PWTd明显高于G3组;G6组体重指数、短轴缩短率、LVEF明显高于G5组,左心房内径、每搏输出量及左心室射血时间、心率、cESS及MEE明显低于G5组。双变量相关分析显示,E'/A'、E/E'与cESS、MEE等各指标间均有相关关系。结论左心室舒张功能障碍的原发性高血压患者MEE水平明显高于舒张功能正常的原发性高血压患者。     

原发性高血压患者心肌能量消耗水平与左心室重构及收缩功能的相关性

目的探讨多普勒超声指标心肌能量消耗(MEE)评估原发性高血压不同左室构型特点以及左室收缩功能的潜在临床价值。方法选取门诊或住院治疗的106例原发性高血压患者,24例健康人为对照组。用多普勒超声心动图测量心脏结构指标、左室收缩功能常规指标(射血分数、短轴缩短率),应用相关公式计算MEE、左室收缩末周向室壁应力(cESS)、左室质量指数(LVMI)、相对室壁厚度(RWT)。根据LVMI和RWT将高血压患者分为左室正常构型组(22例)、向心性重构组(34例)、向心性肥厚组(26例)和离心性肥厚组(24例);分析各组间左室结构、功能的差异,探讨MEE、cESS与左室结构、功能指标的相关性。结果高血压4组cESS均明显高于对照组,其中离心性肥厚组最高;除向心性重构组外,其余高血压3组MEE均明显高于对照组(均P<0.05),离心性肥厚组MEE最高。相关分析显示:MEE、cESS与左室收缩功能指标以及左心室重构指标均明显相关。结论多普勒超声心动图无创检测原发性高血压患者的MEE水平可反映高血压左室不同构型的心肌生物能量消耗特点;MEE、cESS是评价高血压不同构型左室收缩功能的有效指标。     

多普勒超声心动图检测慢性心力衰竭患者心肌生物能量消耗水平的变化及临床意义

目的 分析慢性心力衰竭(心衰)患者的多普勒超声指标心肌生物能量消耗(MEE)与左心室结构指标及其收缩、舒张、整体功能指标及心衰严重程度(NYHA心功能分级)、C反应蛋白(CRP)、N末端B型利钠肽原(NT-proBNP)之间的关系,探讨MEE用于评估慢性心衰心功能状况的临床价值.方法 选择慢性心衰住院患者99例,据左室射血分数(LVEF)值分为LVEF正常的心衰(HFNEF)组37例,LVEF降低的心衰(HFREF)组62例(其中LVEF>35%、<50%及≤35%分别为30例及32例);据NYHA心功能分级分为Ⅱ级(26例)、Ⅲ级(42例)、Ⅳ级(31例);对照组30例.采用多普勒超声心动图检测并计算MEE及常规结构指标,左心室收缩(LVEF、LVFS)、舒张(E/A、EDT、IVRT)及整体功能指标(Tei指数),并测定各组血清CRP、血浆NT-proBNP水平,分析各组间各参数的差异,探讨MEE与上述指标间的相关性.结果 HFNEF组患者MEE水平与对照组差异无统计学意义(P>0.05),HFREF组患者MEE水平较对照组明显增加(P<0.01);慢性心衰组MEE随LVEF的降低及NYHA心功能分级级别的升高而显著增加(P<0.05);双变量相关分析显示,MEE与心室结构及收缩、舒张、整体功能指标、NYHA心功能分级及血清CRP、血浆NT-proBNP水平之间均具有相关性,其中关系最密切的是左心室收缩功能指标,即MEE与LVEF、LVFS均呈明显负相关[分别为r=-0.540、P<0.01,r=-0.454、P<0.01].结论 随左心室收缩功能障碍及心衰程度的加重,慢性心衰患者的MEE水平逐步升高,MEE与现有的心功能评价指标(如LVEF值、NYHA分级、NT-proBNP 等)均呈明显相关,特别与左心室收缩功能指标关系密切.MEE可从心肌生物能量学角度有效评定慢性心衰患者的心功能状况.     

超声对老年急性心肌梗死患者左心室心肌总应变及左心室重构的研究

目的探讨应用超声技术评价老年急性心肌梗死(AMI)患者左心室心肌总应变,及其与左心室重构的相关性。方法选择心肌梗死患者104例,根据冠状动脉造影结果分为左回旋支(LCX)和(或)右冠状动脉(RCA)病变组(LCX/RCA组)31例、单纯左前降支(LAD)病变组(LAD单支组)34例、包含LAD的2支或3支病变组(多支组)39例,另选择性别、年龄相匹配的同期健康体检者40例为对照组。应用二维超声斑点追踪成像测算左心室各节段心肌及整体总应变矢量(ε)及其与左心室短轴平面间的角度(θ),应用实时三维超声心动图测算左心室重构指数(LVRI)。结果与对照组比较,LCX/RCA组左心室前壁ε,LAD单支组下侧壁、下壁ε未见明显减低(P0.05),LCX/RCA组、LAD单支组、LAD多支组其余不同心肌节段ε明显减低(P0.05),且LCX/RCA组下侧壁、下壁θ,LAD单支组前间隔、前壁θ及多支组各部位θ明显升高(P0.05)。与对照组比较,LCX/RCA组、LAD单支组和LAD多支组整体ε、LVRI均显著降低,整体θ显著升高(P0.05)。LCX/RCA组、LAD单支组和多支组整体ε(r=-0.815,P=0.014;r=-0.747,P=0.031;r=-0.768,P=0.024)、θ(r=-0.719,P=0.043;r=-0.763,P=0.021;r=-0.753,P=0.029)均与LVRI呈显著负相关。结论老年AMI患者左心室心肌ε大小及θ能反映局部及整体的心肌应变能力,整体ε、θ与LVRI均呈负相关性。     

经冠脉自体骨髓干细胞移植改善左室重构机制的研究

目的研究自体骨髓单个核细胞(BM-MNC)和间充质干细胞(MSCs)移植对急性心肌梗死(AMI)后心室重构的影响,探讨不同干细胞移植对心室重构影响的机理。方法以小型猪为研究对象,通过球囊导管压迫冠状动脉前降支的方法,建立小型猪AMI动物模型。在AMI 90 min时,经冠状动脉腔内进行自体BM-MNC和MSCs移植。于术前及干细胞移植后28 d,观察心功能、心肌微血管计数、心肌核因子_KB、心肌细胞凋亡、心肌血管内皮生长因子(VEGF)和碱性成纤维细胞生长因子(bFGF)的mRNA表达。与心功能进行相关性分析。结果(1)术后28 d,BM-MNC组、MSCs组EDD均明显低于AMI模型组(P=0.005),EF明显高于模型组(P=0.0001;P=0.0017)。(2)BM-MNC移植组血管数比梗死组及MSCs组增加(梗死区P=0.000 1,边缘区P=0.000 1)。(3)BM-MNC组及MSCs组心肌细胞凋亡率比梗死模型组减少(梗死区P=0.000 1,梗死边缘区P= 0.000 1,正常区P=0.005 2)。(4)BM-MNC组及MSCs组NF-_KB阳性率比单纯AMI模型组显著降低(P=0.001)。(5)梗死模型组、BM-MNC组以及MSCs组的梗死区及梗死边缘区的VEGF基因表达量与正常对照组的相比增加(梗死区P=0.0001;梗死边缘区P=0.000 1)。BM-MNC及MSCs移植组,心肌梗死区的bFGF基因表达量比梗死模型组及正常对照组均显著增加(P=0.000 1)。LVEF与心肌细胞凋亡呈负相关(r=-0.441 1,P= 0.027 3),与心肌NF-_KB负相关(r=-0.579 6,P=0.000 6);与梗死区、边缘区血管数正相关(r=0.775 0,P=0.000 3);与VEGF表达正相关(r= 0.565 1,P=0.018 1);与bFGF表达正相关(r=0.573 5,P=0.016 1)。结论经冠脉自体BM-MNC及MSCs移植均可减轻心肌梗死后左心室重构,改善急性心肌梗死后心功能,增加心肌血管数量,增加梗死区及梗死边缘区VEGF及bFGF表达,减少心肌细胞凋亡。心功能的改善与干细胞移植后增加心肌血管数量、增加心肌VEGF及bFGF表达、减少心肌细胞凋亡以及减少心肌组织NF-_KB水平有关。     

二维斑点追踪超声心动图评价急性心肌梗死患者左心房应变功能

目的应用二维斑点追踪超声心动图评价急性心肌梗死(acute myocardial infarction,AMI)患者左心房应变功能。方法对AMI患者40例及对照组30例采用常规超声心动图测量二尖瓣口舒张期血流频谱E峰,组织多普勒测量二尖瓣环舒张早期e峰,并计算E/e值。存储心尖四腔心及两腔心动态图像,比较两组间左心房储存时期(即左心室收缩期)整体纵向应变峰值,分析AMI组左心房纵向应变与E/e值相关性。结果 AMI组左心房整体纵向应变较对照组减低,差异有统计学意义(P0.01)。AMI患者左心房整体应变与E/e值成显著负相关,差异有统计学意义(r=-0.35,P0.01)。结论左心房纵向应变是评价AMI患者左心室充盈压的一个较好的指标。     

急性心肌梗死急诊介入治疗后辛伐他汀对早期左心室重构的影响

目的探讨急性心肌梗死(acute myocardial infarction,AMI)急诊直接PCI术后使用辛伐他汀对早期左心室重构的影响。方法选择AMI接受急诊直接PCI患者245例,随机分为辛伐他汀治疗组(治疗组)123例和对照组122例。比较2组术后即刻TIMI分级、计算校正TIMI计帧数(cTFC)和心肌Blush分级。采用彩色多普勒超声心动仪分别于发病早期(<24h)、1、2、3周末连续测量、计算左心室形态、构型等指标并进行分析。结果与基线比较,对照组1周末左心室收缩末内径(LVESD)、左心室短轴前半径(Ra)/内径(D)明显升高,2周末左心室舒张末内径(LVEDD)、LVESD、Ra/D、左心室前部心内膜弧长(ASL)、后部心内膜弧长(PSL)明显升高,3周末LVEDD、LVESD、Ra/D、ASL、PSL、LVEF明显升高,差异有统计学意义(P<0.05,P<0.01);治疗组2周末LVEDD、LVESD、PSL、LVEF明显升高,3周末LVEDD、LVESD、ASL、PSL、LVEF明显升高(P<0.05,P<0.01)。与对照组比较,治疗组2周末、3周末LVEDD、LVESD、Ra/D、ASL、PSL明显降低,LVEF明显升高,差异有统计学意义(P<0.05)。结论 AMI患者急诊直接PCI术后,使用辛伐他汀对早期左心室重构有抑制作用。     

急性冠脉综合征患者血浆脑钠素检测及其意义

目的观察急性冠脉综合征(ACS)患者入院时血浆脑钠素(BNP)浓度,分析其与左室射血分数(LVEF)和心肌坏死标记物肌钙蛋白(IcTnI)的相关性,探讨其临床意义。方法73例急性冠脉综合征患者,按临床类型分为急性心肌梗死(AMI)组46例和不稳定性心绞痛(UA)组27例。同时从体检中心选择11例健康体检者作为健康对照组。ELISIA方法检测ACS患者血浆BNP和cTnI浓度,用超声心动图测定左室射血分数(LVEF),比较不同组别差异,并分析BNP与LVEF和cTnI的相关性。结果AMI组平均血浆BNP浓度明显高于UA组和正常对照组(P<0.01),UA组血浆BNP亦高于正常对照组(P<0.01)。AMI组BNP与LVEF呈负相关(r=-0.673,P<0.01),与cTnI呈正相关(r=0.398,P<0.05)。结论ACS患者入院时血浆BNP即明显升高,且各临床类型的血浆BNP水平存在差异,BNP水平不仅可以反映急性心梗患者心功能状态,而且也可以反映心肌坏死程度。     

实时三维超声对心肌梗死患者左室收缩同步性和收缩功能的分析

目的:应用实时三维超声心动图(RT-3DE)评价陈旧性心肌梗死患者左室收缩同步性与收缩功能,并探讨左室收缩同步性与收缩功能的关系.方法:研究对象分为2组:正常组20例,陈旧性心肌梗死组30例,其中陈旧性前壁心肌梗死14例,均行实时三维超声心动图检查,通过脱机软件分析整体及节段容积-时间曲线,获取左室整体及节段收缩功能参数、左室收缩同步性参数,并将左室心肌分为基底段、中间段、心尖段3个水平节段进行分析.结果:心肌梗死组左室收缩末期容积(ESV)、左室舒张末期容积(EDV)显著大于正常组(P＜0.01),左室射血分数(LVEF)显著小于正常组(P＜0.001).心肌梗死组左室16节段收缩同步性参数显著大于正常组(P＜0.001),且均与LVEF呈负相关,其中Tmsv-16-SD与LVEF的相关系数r=-0.644,P＜0.01.与正常组相比,前壁心肌梗死组3个水平节段的Tmsv-sel-SD、Tmsv-sel-Dif增大(P＜0.05),REF明显减小(P＜0.05),其中心尖段Tmsv-sel-SD、Tmsv-sel-Dif与心尖段REF呈负相关(r=-0.656,-0.687,P＜0.05).结论:RT-3DE能定量评价心肌梗死患者左室收缩同步性及收缩功能,左室不同步运动可影响左室收缩功能,前壁心肌梗死患者心尖段心肌的不同步运动与其节段收缩功能减低密切相关.     

门控心肌灌注显像相位分析评价陈旧性心肌梗死患者左心室收缩同步性

目的 应用单光子发射计算机断层成像(SPECT)/CT门控心肌灌注显像(GMPI)相位分析技术评价陈旧性心肌梗死(OMI)患者的左心室收缩同步性,并探讨影响收缩不同步的独立危险因素.方法 选择2010年10月至2013年9月在常州市第一人民医院确诊的OMI患者76例作为OMI组,同时选择健康者74例作为对照组,对其临床资料进行回顾性分析.所有研究对象均进行静息GMPI检查,应用Cedars Sinai QGS软件相位分析技术获得左心室收缩同步性参数[相位直方图带宽(BW)和相位标准差(SD)]以及心功能参数,应用QPS软件获得心肌灌注缺损范围.分别比较OMI组与对照组、左心室射血分数(LVEF)≤35％与LVEF＞ 35％ OMI患者之间的BW和SD值.以对照组BW值的x-±2s为异常临界阈值,大于该阈值定义为左心室收缩不同步,分析其独立危险因素.结果 (1)OMI组的BW[(91.3 ±58.6)°比(37.2±11.7)°,P＜0.001]和SD值[(27.3±20.8)°比(1 1.8±5.4)°,P＜0.001]均高于对照组,LVEF低于对照组(P＜0.001).LVEF≤35％的OMI患者BW[(136.0±52.9)°比(51.0±24.0)°,P＜0.001]和SD值[(38.7±21.3)°比(17.1±14.0)°,P ＜0.001]均高于LVEF＞ 35％的OMI患者.(2)在OMI患者中,左心室收缩不同步(BW ＞60.6°)的比例为57.9％ (44/76).与左心室收缩同步性正常OMI患者比较,不同步患者的LVEF较低(P＜0.0O1),左心室舒张末期容积、收缩末期容积、室壁运动异常总积分、室壁增厚异常总积分和心肌灌注缺损范围均较高(P均＜0.001).(3)LVEF≤35％的OMI患者合并左心室收缩不同步的比例高于LVEF＞35％的患者[91.7％ (33/36)比27.5％ (11/40),P＜0.001].(4)Pearson线性相关分析显示,LVEF与BW呈负相关(r=-0.807,P＜0.001).(5)多因素logistic回归分析显示,心肌灌注缺损范围是导致OMI患者发生左心室收缩不同步的独立危险因素(OR=1.076,95％ CI:1.015 ～1.141,P=0.015).结论 GMPI相位分析可客观反映左心室收缩同步性;OMI患者左心室收缩同步性减低,左心室收缩不同步与LVEF相关;心肌灌注缺损范围是OMI患者发生左心室收缩不同步的独立危险因素.     

Perforation of the Right Ventricle After Endomyocardial Biopsy Detected by Color Flow Doppler Echocardiography

Right ventricular perforation after endomyocardial biopsy of a heart transplant patient was established by color flow Doppler echocardiography. Systolic filling and diastolic drainage of the pericardium were seen. Healing of the perforation occurred spontaneously with no Doppler signs of perforation 8 days later.     

Respective role of sympathetic tone and of cardiac pauses in the genesis of 62 cases of ventricular fibrillation recorded during Holter monitoring

Sixty-two Holter recordings of sudden death due to ventricularfibrillation (VF) were analysed by full disclosure and computerizedprocessing. Thirteen sudden deaths were due to torsades de pointesin non coronary subjects (11/13), related to quinidine-likedrugs and/or hypokalaemia: they were always initiated by a longRR cycle due to a post-extrasystolic pause, and announced bya progressive decrease of mean heart rate (from 77.5 ±2.5 to 60.6 ± 2.7 beats min^–1, P<0.001), inthe three preceding hours. The other cases occurred in coronarypatients (45/49), with acceleration of ventricular tachycardia( VT), monomorphic in 24 cases, polymorphic in 13, the ventricularrate increasing from 220.6 ±55 to 241.5 ±69 beatsmin^–1, rather than with primary VF (12 cases). A cardiacpause (RR cycle exceeding 125% of the mean five preceding cycles)was present in 22/49 cases immediately before the onset of VT/VF.The coupling interval of the extrasystole initiating VT/ VFwas shorter than the shortest value encountered before: 377.6±± 94.5 ms vs 421.4 ± 92.3. The prematurityindex (coupling interval/preceding RR cycle ratio) was lowerin primary VF than in VT leading to VF. In the last hour precedingVF, ST changes were unusual (five cases), whereas heart rateincreased from82.8±20 to 92.0 ± 26.7 beats min^–1,(P<0001).This acceleration was in fact present only in caseswithout pauses before the onset of VT/VF: from 85.0±22.8to 99.1 + 31.1 (n = 27, P<0.001) whereas no changeoccurredin cases with preceding pause: from 79.8 ±15.5 to 80.8±16.3 (n = 22, P = NS). As a result, VT/VF without apreceding pause occurs in the setting of a higher heart rate,most probably reflecting a higher sympathetic drive. Preventionof these two main determinants by pacing and beta-blocking therapyshould bemore efficient than the use of antianginal or antiarrhythmicdrugs.     

老年患者血清护骨素水平与左心室结构和功能的相关性研究

目的探讨老年患者血清护骨素水平对于心脏左心室结构与功能的预测意义。方法选择51 7例老年患者,根据护骨素水平按3分位数分组:护骨素<1.50μg/L组(A组,171例)护骨素1.50～2.72μg/L组(B组,176例),护骨素>2.72μg/L组(C组,1 70例)。ELISA法检测血清护骨素水平;多因素采用多元逐步回归及logistic回归分析。结果随护骨素水平升高,3组LVEF逐渐下降(P<0.01),左心室质量指数逐渐升高(P<0.01),以左心室肥厚为因变量,以性别、年龄、收缩压、舒张压、空腹血糖、血肌酐、TC,LDL-C.HDL-C、TG、sqrt护骨素为自变量,logistic回归分析显示,左心室肥厚与性别、年龄、收缩压、sqrt护骨素独立相关。结论在老年心血管病患者中,血清护骨素水平可能是左心室肥厚的独立危险因素,并且老年女性发生左心室肥厚的风险高于男性。     

Premature ventricular beats in a previously healthy child

A 12-year-old girl presented to the emergency department with a chief complaint of left-sided chest pain. On physical examination she was noted to have an irregular pulse, and an electrocardiogram revealed 30 to 50 premature ventricular contractions per minute with periods of bigeminy. The patient was admitted to the intensive care unit and treated with antiarrhythmic medication without resolution of her premature ventricular contractions. A diagnostic workup, including echocardiogram, Holter monitoring, and exercise stress testing, was performed. It was determined that the cardiac dysrhythmia, consisting of unifocal premature ventricular contractions with a characteristic configuration on the electrocardiogram, was benign in nature and did not require antiarrhythmic therapy.     

Impact of revascularization in patients with post‐infarction left ventricular aneurysm and ventricular tachyarrhythmia

BackgroundVentricular arrhythmia is a leading cause of cardiac death among patients with post‐infarction left ventricular aneurysm (PI‐LVA). The effect of coronary revascularization in PI‐LVA patients with ventricular tachyarrhythmia remains unknown. This study aims to investigate the impact of revascularization therapy on clinical outcomes in these patients.MethodsA total of 238 PI‐LVA patients were enrolled, and 59 patients were presented with sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). Patients were classified into 4 groups by treatment strategies (medical or revascularization) and the presence of VT/VF: group 1 (n = 57): VT/VF− and revascularization−; group 2 (n = 122): VT/VF− and revascularization+; group 3 (n = 34): VT/VF+ and revascularization+; and group 4 (n = 25): VT/VF+ and revascularization‐. The clinical outcomes were compared, and the primary endpoint was cardiac death or heart transplantation.ResultsPatients were followed up for 45 ± 16 months, and 41 patients (17.2%) reached the primary endpoint. Kaplan–Meier analysis showed that in VT/VF− patients, revascularization associated with higher cardiac survival compared with medical therapy (log‐rank p = .002), but in VT/VF+ patients, revascularization did not predict better cardiac outcome (log‐rank p = .901). Cox regression analysis revealed PET‐EF (HR 4.41, 95% CI: 1.72–11.36, p = .002) and moderate/severe mitral regurgitation (HR 2.32, 95% CI: 1.02–5.30, p = .046) as independent predictors of adverse cardiac outcome in patients with VT/VF.ConclusionPI‐LVA patients with VT/VF are at high risk of adverse cardiac outcome, and coronary revascularization does not mitigate this risk, although revascularization was associated with higher cardiac survival in PI‐LVA patients without VT/VF.