背向散射技术与SPECT对急性前间壁心肌梗死的评价

目的：观察在急性前间壁心肌梗死中梗死区心肌超声背向散射参数变化，并研究其与单光子发射型计算机断层扫描（SPECT）所测相应心肌节段灌注缺损值的关系。方法：心肌梗死组20例，对照组15例，均于冠状动脉造影术后第4～5天行超声背向散射参数分析及SPECT。结果：与正常对照组比较，心肌梗死组梗死区心肌标化背向散射积分值明显增高，背向散射积分周期变化幅度（CVIB）减低，周期变化延迟时间校正值延长。梗死区心肌CVIB与SPECT相应节段心肌血流灌注缺损值呈负相关。结论：背向散射技术与SPECT在冠心病心肌缺血诊断中具良好的一致性，是一种无创评价心肌缺血的新方法。     

IBS对早期糖尿病心脏病变的超声心动图检测

目的 探讨背向散射积分技术(IBS)在评价早期糖尿病心脏病变左室功能方面的临床应用价值.方法 检测36例糖尿病患者和22例健康人心室舒张早期快速充盈波E峰峰值流速(E);心房收缩充盈波(A);E/A值,用Simpson法测量左室射血分数(EF).再记录左室室间隔和后壁中部心肌层内的平均IBS(AII)和IBS的周期变异幅度(CVIB),将标化平均心肌IBS定义为心肌AII\心包AII(IBS%).结果 左室舒张早期充盈峰值速度与心房收缩期充盈峰速度(E),左室舒张早期充盈峰值速度与心房收缩期充盈峰值速度的比值(E/A),左室射血分数(EF)差异均无统计学意义;左室心房收缩期峰值充盈速度(A)(68.00±10.08)高于对照组(60.17±90.45)差异有统计学意义(P<0.05),糖尿病组间隔心肌背向散射积分的标化值(IBS%)(58.8±9.13)高于对照组,左室后壁的背向散射积分周期变异幅度(CVIB)(6.57±1.46)低于对照组,两者均具有统计学的显著意义(分别为P<0.05,P<0.01) 结论 IBS技术为临床早期检测出糖尿病心脏病变左室功能变化提供了一种无创性方法,对于早期糖尿病心脏病变的患者,间隔的IBS%和左室后壁的CVIB是更敏感的IBS指标.     

声学密度定量技术与冠状动脉造影术的对比研究

目的：探讨声学密度定量（AD）技术评价正常、狭窄及闭塞血管支配区域心肌的组织特征。方法：对疑诊冠心病的64例患者，根据冠状动脉造影结果将192支冠状动脉分组：正常组（A组）、狭窄组（B组）、闭塞组（C组），检测其相应血管支配区域心肌的背向散射积分参数。结果：与A组相比，B组心肌的背向散射积分的标化值（IBS％）增高；而背向散射积分周期变化幅度（CVIB）减小；C组心肌的IBS％增高更明显；CVIB减小也更明显。且14支闭塞血管支配区域心肌的CVIB曲线与正常节段呈反向，N－delay在B组及C组明显延长，同一参数组间比较差异均有显著性（P＜0．01），结论：AD技术能客观反映正常，狭窄及闭塞冠状动脉脉供血区域心域心肌的不同组织特性变化，对鉴别冠心病不同病变心肌的灌流特征具有一定的诊断意义。     

应用背向散射积分技术检测急性心肌梗死的实验研究

目的　探讨超声组织定征 (UTC)背向散射积分 (IBS)技术对实验动物急性心肌梗死(AMI)的诊断价值。方法　HP550 0型超声诊断仪及S8探头 ,健康雄性小猪 1 2只 ,全麻下行冠脉左前降支 (LAD)闭塞 ,分别于术前、术后 1、2小时及 1周获取胸骨旁左室长轴、乳头肌短轴、心尖四腔和两腔的标准切面图像 ,测定IBS值、背向散射积分周期变化 (CVIB)、IBS周期变化跨壁梯度(TGCVIB)、周期变化延迟时间 (DTCV)及室壁增厚率 (△T % )的变化。结果　术后 1小时IBS %明显升高 ,DTCV %延长 ,CVIB %、TGCVIB和△T %明显降低 ;术后 2小时与 1小时无明显差别 ;术后 1周IBS %、DTCV %升高更明显 ,CVIB %、△T %减低更明显 ,而TGCVIB为负值。前壁IBS %、CVIB %分别与△T %行相关分析 ,相关系数分别为r =- 0 55 ,r =0 62 (P均 <0 0 1 ) ,DTCV %△T %也有一定的相关性 ,r =- 0 46(P <0 0 5)。结论　UTC背向散射技术可用于检测实验动物急性冠状动脉闭塞后心肌组织声学特征的改变 ,有助于AMI的诊断     

高血压患者左室重构的组织定征及其与功能改变之间的关系

为观察高血压患者不同左室构型的心肌背向散射积分(IBS)参数的变化 ,并分析其与左室功能改变之间的关系 ,我们比较 2 7例健康志愿者和 14 4例原发性高血压患者不同左室构型心肌IBS及其周期变异率 (CVIB)的差别 ,并分析其与心肌收缩期、舒张早期和晚期峰值速度 (VS、VE、VA)以及     

肥厚型心肌病心肌超声组织定征背向散射技术的研究

目的：比较肥厚型心肌病（HCM）患者与正常人左室后壁（LVPW）心肌声学特性是否存在差异，并探讨超声组织定征（UTC）技术在评价HCM方面的价值。方法：应用UTC背向散射积分（IBS）测定法分别HCM组（38例）和正常对照组（40例）LVPW，室间隔（IVS）部位的心肌IBS参数。结果：两组IVS心肌，LVPW心肌IBS的相对值（IBS％），IBS的周期变化（VCIB）均有显著性差异（P＜0．05），HCM组IVS，LVPW均存IBS，CVIB的跨壁梯度，而正常对照组则无，结论：HCM患者LVPW心肌IBS参数与正常人不同，其测定是一种客观评价HCM的UTC方法。     

小剂量多巴酚丁胺负荷超声与心肌背向散射积分检测存活心肌的对比研究

小剂量多巴酚丁胺负荷超声(LDDSE)作为一种评价心肌存活性的方法，主要通过观察异常节段室壁运动的改善来评判存活心肌，存在一定主观性。而心肌背向散射积分(IBS)通过检测心肌结构和功能改变所引起背向信号的变化，推测心肌的病理变化，从而能无创地评价心肌存活性。本研究通过观察LDDSE中存活心肌IBS参数的变化，探讨IBS检测存活心肌的潜力。     

多普勒组织成像定量分析心脏介入前后心功能的变化

目的 采用脉冲波多普勒组织成像技术(PW-DTI)观察急性心肌梗死(AMI)患者心脏介入治疗前后梗死局部室壁和二尖瓣环的运动变化,定量分析左心室局部与整体的心功能.方法 30例急性心肌梗死患者,于发病7～10d内行择期介入治疗,采用PW-DTI分析介入治疗前、后室壁梗死区域和二尖瓣环DTI指标:收缩期波峰值速度(Vs)、舒张早期波峰值速度(Ve)、舒张晚期波峰值速度(Va)及舒张早期波峰值速度/舒张晚期波峰值速度(Ve/Va),再与27名健康成人作对照分析.结果 急性下壁和急性前壁心肌梗死患者术前与健康人比较:梗死区域各室壁Vs、Ve和Ve/Va均显著降低(P＜0.01);心梗患者介入治疗前后比较:与梗死区域相对应的室壁运动恢复明显,Vs、Ve和Ve/Va均显著增高(P＜0.01).反映左心室整体心功能的指标二尖瓣环部位的Vs、Ve和Ve/Va在所有心梗患者术前均较健康人显著降低(P＜0.01),介入治疗术后较术前显著增高(P＜0.01).结论 DTI能够定量检测梗死区心肌的运动异常和介入治疗后再灌注心肌的运动变化,监测介入治疗前后局部和整体的心功能,为术后疗效的判定提供了新的定量指标.     

超声背向散射积分评价兔慢性肾功能衰竭心肌损害的实验研究

<正>超声背向散射积分技术(integrated backscatter,IBS)是新近发展较快的一项超声组织定征技术,该技术能够对心肌的结构和功能特性提供量化信息[1],为无创性检测心肌病变提供了一种有效手段。目前,该技术评价尿毒症心肌病变已有相关报道,但评价慢性肾功能衰竭(chronic renal failure,CRF)进展中心肌病变的研究鲜有报道。本研究以病理为对照,观察CRF发生发展过程中心肌背向散射积分参数的变化,为应用IBS技术正确评价及早期发现CRF心肌损害提供实验依据。     

颈动脉粥样硬化内中膜的超声背向散射积分分析

目的应用超声背向散射积分技术评估颈动脉粥样硬化内中膜的组织特性。方法 38例颈动脉粥样硬化患者及正常对照组26例分别对不同部位的颈动脉内中膜进行测量,并检测其背向散射积分值,对其进行对比分析。结果背向散射积分测定颈动脉粥样硬化组各部位内中膜IBS值均高于正常组,差异具有统计学意义(P<0.01)。结论背向散射积分技术反映组织内部结构声学特性,能较好的评估粥样硬化内中膜的组织特性。     

儿童心肌背向散射积分的应用研究

目的:探讨心肌背向散射积分(IBS)在儿童中的应用价值。方法:检测50例正常儿童(对照组)及16例心肌病儿童(心肌病组)基底段前间隔、后间隔、左室侧壁、左室后壁的平均IBS值(AII)和周期变化幅度(CVIB)值。结果:所测心肌4个节段的AII%,各年龄组间及性别间比较差异无统计学意义(均P>0.05)。后壁心包AII>侧壁心包AI(IP<0.05)。各节段心肌AII%接近正态分布。各节段心肌间两两比较,前室间隔与后室间隔、侧壁与后壁AII%差异无统计学意义(均P>0.05)。前室间隔、后室间隔AII%小于侧壁和后壁AII%(均P<0.01)。各节段心肌CVIB比较差异无统计学意义(均P>0.05)。心肌病组与对照组比较,心肌节段AII%明显升高(P<0.05)、CVIB明显下降(P<0.01)、IBS曲线平坦。结论:正常儿童心肌各节段AII%及CVIB值测量可为儿科临床进行各种心肌病变的组织定征及定量分析提供参考依据。心肌病患儿AII%升高、CVIB下降、IBS曲线形态异常。     

Electrophysiologic effects of bepridil in normal and infarcted canine myocardium

The electrophysiologic effects of bepridil, 10 mg/kg i.v., were determined in normal noninfarcted and in infarcted ventricular myocardium in 8 urethane-anesthetized dogs 4-6 days after anterior myocardial infarction. At drive cycle lengths of 400 and 333 ms, bepridil significantly increased relative (RRP) and effective (ERP) refractory periods in both normal ventricular tissue (mean increases, RRP 7-14%, ERP 5-6%, p less than 0.05-0.01) and in infarcted ventricular tissue (mean increases, RRP 12-15%, ERP 13-14%, p less than 0.01). Bepridil also selectively prolonged the local activation delay in infarcted ventricular myocardium (mean increases 37.5-45.1%, p less than 0.01), while ventricular excitation thresholds were not altered by bepridil in either normal or infarcted myocardium. Before bepridil administration, programmed ventricular stimulation initiated sustained ventricular tachycardias in 6 of the 8 postinfarction dogs tested. After bepridil, 2 of the 6 previously responsive animals were rendered noninducible, 3 animals responded to programmed stimulation with nonsustained tachyarrhythmias of relatively slower rates, and the one remaining dog responded with sustained ventricular tachycardia (VT). These data suggest that increases in refractoriness in both normal noninjured and in ischemically injured ventricular tissue, with a selective delay in conduction in ischemically injured tissue, contribute to the antiarrhythmic actions of bepridil in the setting of myocardial infarction.     

S-甲基异硫脲抑制梗塞兔心肌诱导型一氧化氮合酶的表达

目的　研究S 甲基异硫脲 (SMT)对梗塞兔心肌组织内诱导型一氧化氮合酶 (iNOS)活性的抑制作用。方法　对左房心耳和心尖中间弯曲的冠状动脉前外侧枝进行结扎 ,建立心肌梗塞模型。应用L 精氨酸转换为L 胍氨酸法测定家兔心肌梗塞区和非梗塞区诱导型一氧化氮合酶的活性 ,同时观察S 甲基异硫脲和NW 硝基 L 精氨酸 (L NNA)对诱导型一氧化氮合酶活性的抑制作用。结果　冠状动脉结扎后 48h、72h和 96h ,心肌梗塞区诱导型一氧化氮合酶活性比非手术组显著增加 (P <0 0 1) ,并在 72h达到峰值 ;梗塞后 72h左室壁cGMP含量也明显增加 (P <0 0 1) ;同时SMT能明显降低梗塞区心肌诱导型一氧化氮合酶的活性 (P<0 0 1)。结论　SMT能明显抑制梗塞兔心肌iNOS的活性 ,提示SMT对改善心脏功能和治疗急性心肌梗塞具有一定的临床效果。     

钙通道阻滞剂对心肌重构保护机制的研究

目的研究L和L/T型钙通道在梗死心肌组织中钙蛋白酶介导的心肌损伤中的作用。方法结扎大鼠左冠状动脉建立心肌梗死模型,术前7d分别用安慰剂、L型钙通道阻滞剂阿莫地平(4mg·kg-1d-1)、L/T型钙通道阻滞剂米贝拉地尔(10mg·kg-1·d-1)。术后1、3、7、14d分别检测左心室游离壁(LVFW)、室间隔(IS),右室壁(LV)钙蛋白酶(ucalpain,mcalpain)及钙蛋白酶抑制蛋白(calpastatin)表达。术后14d测心肌梗死病灶大小、IS隔厚度、左室大小。结果室间隔ucalpain蛋白表达于心肌梗死14d增加;左室游离壁mcalpain蛋白表达于心肌梗死3d时达高峰。米贝拉地尔更明显地抑制心肌组织mcalpain的上调,缩小心肌梗死病灶。阿莫地平则抑制ucalpain蛋白表达,明显抑制左室扩张和室间隔肥厚。结论心肌梗死病理过程中,梗死病灶内mcalpain上调,肥厚组织中ucalpain上调。L和L/T型钙通道阻滞剂能减轻心肌重构与选择性的抑制心肌组织中的ucalpain和mcalpain有关。     

Neutrophil depletion suppresses 111In-labeled platelet accumulation in infarcted myocardium

Platelets and neutrophils accumulate rapidly in infarcted myocardium. Although antineutrophil agents reduce the size of the infarcted area, this is not observed with antiplatelet drugs. The possibility that myocardial ischemia-induced platelet deposition was secondary to a neutrophil-mediated event was assessed by injecting prostacyclin-washed autologous 111In-labeled platelets and measuring the amount of radioactivity in different regions of the heart following 90-min occlusion of the left anterior descending coronary artery followed by reperfusion for periods up to 5 h. Platelet deposition during the reperfusion phase was linear with time and similar to the time course of neutrophil accumulation. There was a transmural distribution of radioactivity across the myocardium where the "zone" between infarcted and risk regions, called the "interface," greater than infarct greater than risk greater than normal. Neutropenia (21 +/- 2% control levels), induced with specific sheep anti-dog neutrophil antiserum, had minimal effects on platelet aggregation ex vivo, but significantly reduced platelet accumulation in the ischemic myocardium following 5-h reperfusion and abolished the transmural platelet distribution. These results suggest that myocardial platelet deposition is secondary to a neutrophil-mediated event in this occlusion-reperfusion model of myocardial injury. Interactions between platelets and neutrophils at the site of tissue damage may influence the process of myocardial ischemic injury.     

屏气电影法MRI评价存活心肌的初步研究

目的探讨MRI屏气电影成像技术评价存活心肌的价值。方法应用屏气电影法MRI和心肌首过灌注MRI对24例受检者进行检查，分析局部心功能的变化，并将屏气电影法MRI的结果与心肌首过灌注MRI进行比较。结果16例心梗患者的梗死节段室壁运动及室壁厚度异常，在梗塞心肌区内，可逆心肌的心肌增厚牢显著高于不可逆心肌。结论屏气电影法MRI对存活心肌的评价具有重要价值。     

Calcium channel blockade limits transcriptional,translational and functional up-regulation of the cardiac calpain system after myocardial infarction

Abnormal Ca(2+) inward current through cardiac Ca(2+) channels during ischemia has been shown to be an initial signal for activation of myocardial Ca(2+)-dependent enzymes. This study investigated the contribution of cardiac L- and T-type Ca(2+) channels in the calpain-mediated myocardial damage following myocardial infarction. Myocardial infarction was induced by permanent ligation of the left coronary artery. Infarcted rats were orally treated with placebo, amlodipine (L-channel blockade; 4 mg/kg/day) or mibefradil (L-/T-channel blockade; 10 mg/kg/day) beginning 7 days before induction of myocardial infarction. Gene expression, protein levels and enzyme activity of calpains I and II were measured 1, 3, 7 and 14 days postcoronary occlusion in the noninfarcted and infarcted myocardium. Infarct size, left ventricular dilation and interstitial collagen volume fraction were determined in picrosirius red-stained hearts. Myocardial infarction induced an up-regulation of calpain I mRNA, protein and activity in the noninfarcted myocardium (maximum 14 days postinfarction), whereas mRNA, protein and activity of calpain II were maximally increased in the infarcted myocardium 3 days postinfarction. Fourteen days postinfarction, infarct size was 49%, the left ventricle was dilated and interstitial collagen volume fraction was increased. Amlodipine-inhibited mRNA, protein and activity up-regulation of calpain I decreased interstitial collagen volume fraction and infarct size. Mibefradil-attenuated mRNA, protein and activity up-regulation of calpain II at all four time points measured and of calpain I at 7 and 14 days postinfarction reduced infarct size and prevented left ventricular dilation. Infarction-induced cardiac hypertrophy was accompanied by an up-regulation of calpain I, whereas calpain II was up-regulated in the infarcted myocardium. Cardiac L- and T-type Ca(2+) channel blockade differentially reduced postinfarction remodeling associated with selective inhibition of cardiac calpains I and II, respectively.     

Dantrolene: effects on abnormal intracellular Ca(2+) handling and inotropy in postinfarcted rat myocardium

The present study was designed to investigate the effects of dantrolene on intracellular Ca(2+) ([Ca(2+)](i)) handling and inotropy in rat infarcted myocardium. Dantrolene-treated rats with myocardial infarction were placed into two different dosage groups. The infarcted control group received placebo only. Isometric contractility and intracellular Ca(2+) transients were recorded simultaneously in isolated papillary muscles. Diastolic [Ca(2+)](i) was significantly lower in muscle preparations from infarcted rats receiving dantrolene compared to the placebo control group. Additionally, treatment with dantrolene in infarcted rats significantly improved the inotropic response to 10(-4) M isoproterenol. The protein levels of the sarcoplasmic reticulum Ca(2+) ATPase were increased in infarcted rat hearts with dantrolene treatment. We conclude that dantrolene improved the inotropic response to beta-adrenoceptor stimulation in rat postinfarcted myocardium, which is related to improved intracellular Ca(2+) handling, and lowered diastolic Ca(2+) concentration.