心肌实时超声造影定量评价犬急性心内膜下心肌缺血

目的 探讨心肌实时超声造影技术在急性心内膜下心肌缺血诊断和预测梗死透壁程度中的价值.方法 栓塞微球通过冠状动脉介入技术注射入9只试验犬左冠状动脉回旋支诱发心肌缺血.分别在基础状态和栓塞后 5 min、60 min以及 120 min,应用自制造影微气泡进行胸骨旁乳头肌中部水平心肌实时超声造影,对节段心肌造影强度-时间曲线进行指数方程y=A*(1-exp-k*t)+B拟合.4 h后TTC染色法确定室壁最终梗死程度.结果 冠状动脉注射微球后,19个节段室壁心内膜下心肌3个时间点的A*k标化值均明显降低(P<0.05),对应心外膜下心肌变化不明显(P>0.05).19个节段室壁收缩期增厚率栓塞前后差异无统计学意义(P>0.05).60和120 min时的A*k值有一定程度升高,且与最终心肌梗死面积的负相关系数(r=-0.94,P<0.001)高于 5 min时(r=-0.71,P=0.03).结论 心肌实时超声造影定量参数能够敏感准确地反映心内膜下心肌缺血或梗死程度.     

速度向量成像结合心肌超声造影评价犬急性心肌缺血局部心肌功能

目的 探讨速度向量成像技术评价急性心肌缺血后左心室局部心肌收缩功能改变的价值.方法 健康杂种犬10只,开胸并于第一对角支1 cm以下套扎左冠状动脉前降支,分别在套扎前基础组、套扎30分钟后缺血组,用超声心动图速度向量成像技术记录左室局部心肌收缩期峰值速度(VSYS),峰值应变(SSYS)、峰值应变率(SRSYS),用声诺维进行实时心肌超声造影(MCE),对局部室壁心肌造影强度-时间曲线进行指数方程Y=A·(1-exp-k·t)拟合.结果 与基础组比较缺血节段心肌血流灌注异常,标化后的A·K值明显减低(P<0.05),长轴方向上收缩期VSYS、SSYS、SRSYS均明显减低(P<0.001).结论 长轴方向上收缩期峰值速度,应变、应变率能够准确、敏感地发现急性心肌缺血导致的局部心肌收缩功能障碍.     

心肌运动速度和应变率评价不同程度心肌缺血

目的应用定量组织速度成像(QTVI)技术检测犬不同程度急性心肌缺血前后左室前壁心肌运动速度和应变率(SR)的变化，探寻一种能定量、敏感、无创性地评价左室局部收缩及舒张功能的新方法。方法将9只开胸犬冠状动脉左前降支(LAD)血流减少造成中度、重度心肌缺血模型，取左室乳头肌水平短轴观，以QTVI分别检测不同程度缺血时左室前壁心内膜下心肌和心外膜下心肌收缩期峰值运动速度(Vsendo、Vsepi)、舒张早期峰值运动速度(Veendo、Veepi)，并计算出收缩期SR(SRs)和舒张早期SR(SRe)。结果基础状态下，心内膜下心肌速度高于心外膜下心肌速度。缺血导致左室前壁Vsendo、Veendo、Veepi和SRe均显著下降，尽管Vsepi降低不明显，但SRs降低显著。结论心肌运动速度和应变率能敏感地评价不同程度实验性心肌缺血，比常规的方法(运动幅度和室壁增厚率)更敏感。     

应变及应变率成像评估心肌桥患者局部心肌缺血的价值

目的探讨定量组织速度成像和应变及应变率评估冠状动脉心肌桥引起局部心肌缺血的临床价值。方法冠状动脉前降支心肌桥患者47例(心肌桥组)与冠状动脉正常者40例(对照组),测量前降支支配区域9个节段的收缩期峰值速度、峰值应变及应变率、舒张早、晚期峰值速度、舒张早、晚期峰值应变及相应的应变率。结果与对照组比较,心肌桥组前间隔各节段、前壁基底段及中间段、后间隔中间段收缩期峰值速度及峰值应变率明显减低(P<0.05);前间隔基底段和中间段舒张早期、晚期峰值速度及舒张早期峰值应变率明显减低(P<0.05);前壁基底段、前间隔各节段收缩期峰值应变,前壁、前间隔舒张晚期峰值应变明显减低、侧壁心尖段明显升高(P<0.05)。结论定量组织速度成像和应变及应变率可定量检测冠状动脉心肌桥引起的心肌缺血。     

腺苷负荷实时心肌超声造影诊断心肌缺血

目的探讨应用实时心肌超声造影技术(RT-MCE)结合腺苷负荷试验检测缺血心肌的价值。方法在开胸犬中结扎左冠状动脉前降支(LAD)建立心肌缺血及梗死模型。分别采集基础状态、缺血状态及梗死状态下的RT-MCE图像,然后于三种状态下给予腺苷140μg.kg-1.min-1持续静脉微量泵注射6 min,重复上述记录。利用Qlab分析软件得出左室16节段的时间-强度曲线,测量在负荷前后平台期心肌显影强度(A)、曲线上升斜率(β)及A.β的变化。结果在基础状态下,冠状动脉各节段应用腺苷后A、β及A.β较用药前均显著增加(P<0.05)。在LAD节段,基础状态与缺血状态的A、β及A.β值差异无统计学意义(P>0.05),应用腺苷后缺血部位A值呈降低趋势,β及A.β略增加,但差异无统计学意义(P>0.05);梗死状态下,LAD节段的A、β及A.β值均较基础状态及缺血状态显著性降低(P<0.01,P<0.05),应用腺苷后A、β及A.β值较用药前差异无统计学意义(P>0.05)。结论实时心肌超声造影技术结合腺苷负荷试验可以定量检测缺血心肌,具有重要的临床应用价值。     

心肌声学造影评价心脏X综合征患者的价值

目的 应用心肌声学造影评价心脏X综合征患者的价值.方法 选取心脏X综合征50例患者与29例正常人经心肌声学造影(MCE)的同时应用超声心动图得到以下参数:造影剂峰值密度(A)、心肌血流速率β、心肌血流容积(MBF MBF=A×β)左室舒张末期内径LVEDD(mm)、左室收缩末期内径LVESD(mm)、射血分数EF(%)、舒张早期峰值血流速度E(cm/s)、舒张晚期峰值血流速度A(cm/s)、舒张早期峰值血流速度与舒张晚期峰值血流速度比值E/A、舒张早期血流延迟时间Dt(ms).采用定量分析的方法利用统计学方法对相应节段的心肌灌注情况和心脏功能与正常对照组进行比较.结果 与正常对照组比较,X综合征组β及MFB均显著下降,心脏超声心动图在LVEDD、LVESD、EF、E、A、E/A、Dt,无明显差别.结论 心脏X综合征组患者较正常人血流速度减慢的基础上存在着微循环的损伤,但是并没有导致心脏收缩舒张功能异常.MCE可为心脏X综合征的诊断提供新的诊断依据.     

超声斑点追踪显像技术评价缩窄性心包炎患者左心室局部心肌收缩功能

目的应用超声斑点追踪显像技术(STI)评价缩窄性心包炎(CP)患者左心室局部心肌收缩功能。方法采集26例CP患者左心室心尖位四腔切面、两腔切面、左心室长轴高帧频图像,测量左心室游离壁(前侧壁、下侧壁、前壁、下壁)心内、外膜下心肌各个节段的二维纵向收缩期应变峰值,并与37例正常人比较。结果 (1)CP患者左心室游离壁心外膜下心肌各节段纵向收缩期应变峰值较对照组明显减低(P<0.05),且绝大多数节段P<0.01;(2)CP患者左心室游离壁心内膜下各节段心肌纵向收缩期峰值应变与对照组比较,差异无统计学意义(P>0.05)。结论超声二维应变成像技术能够准确地定量评价CP患者左心室游离壁心内膜下及心外膜下心肌收缩功能,CP患者左心室游离壁心外膜下心肌纵向收缩期峰值应变减低,提示心外膜下心肌收缩功能受损。     

选择性心肌超声造影对冠状动脉与左心室腔间侧支循环的观察与评价

目的采用经冠状动脉选择性心肌超声造影（MCE）观察冠状动脉与左心室腔间侧支循环,并探讨其对于心肌缺血的意义。方法对26例冠心病患者及10例冠状动脉造影正常者的经冠状动脉内MCE进行回顾性分析,检出造影剂直接由心肌进入左心室腔的病例,测量局部节段灌注（minivalue）,应用组织速度显像（TVI）测量相关节段收缩峰值速度（Sm）及与正常节段达峰时间差别（Ts-dif）。结果冠状动脉正常组未见冠状动脉与左心室腔间的侧支循环;冠心病组7例患者总计15个节段可见造影剂直接由心肌进入左心室腔,局部节段minivalue、Sm低于正常节段,但上述指标及Ts-dif优于缺血不伴侧支循环的节段。结论经冠状动脉选择性MCE能够清晰观察心肌内冠状动脉与心室腔间的侧支循环,此侧支循环可在一定程度上改善缺血心肌的收缩功能及心肌灌注。     

VVI及对比超声评价犬冠状动脉狭窄时心肌灌注和舒张功能的关系

目的 应用速度向量成像(VVI)结合心肌声学造影(MCE)评价犬冠状动脉狭窄静息和负荷状态下心肌组织灌注和舒张功能的关系.方法 制作不同程度冠状动脉(前降支)狭窄模型8只,在冠状动脉狭窄前后于静息和多巴酚丁胺注射达峰值剂量时,取左心室短轴图像行VVI分析,并行MCE测量心肌血流量(A·β值)和短轴圆周方向上的舒张期峰值应变率(SRdia),评价二者之间的相关性.结果 静息状态下,冠状动脉轻、中度狭窄时,供血区SRdia和A·β值与正常区差异无统计学意义;重度狭窄时,供血区SRdia和A·β值均低于正常区(P<0.05).多巴酚丁胺负荷下,轻、中度冠状动脉狭窄时,供血区SRdia和A·β值即低于正常区(P<0.05);重度狭窄时,缺血区SRdia和A·β值较正常区降低得更加明显(P<0.05).无论静息还是负荷状态下,SRdia和A·β间均呈正相关(r静息=0.57,r负荷=0.72,P<0.01).结论 VVI技术能够用于评价短轴心肌节段舒张功能,且能在一定程度上反映心肌血流灌注的变化情况.     

心肌声学造影界定急性心肌缺血面积的实验研究

目的应用声学造影剂确定急性缺血心肌的临界点,探讨对心肌缺血面积的估测作用。方法选择健康杂种犬12只,建立开胸犬急性心肌缺血动物模型,经静脉注射声诺维造影剂并进行心肌声学造影(MCE)检查。在左心室心尖长轴二腔心切面,应用MCE的彩色M型曲线技术检测急性缺血心肌分别在前壁和下壁的临界点,以此为界在二维图像上描计出声诺维造影剂灌注缺损面积。启动Q-analysis软件,在左心室心尖长轴二腔心切面,将取样点置于心肌缺血区、临界区及正常心肌组织区,动态追踪此感兴趣区,选择每一心动周期舒张末期图像纳入分析,软件自动生成灌注强度曲线并拟合函数:Y=A(1-eβ2t)+C,得出曲线峰值强度(A),曲线斜率(β)和灌注量(A.β),每个区域的参数均取3次测量的平均值。通过计算局部组织蓄积的最大微泡数量(A)和造影剂在局部充填的速度(β)测定心肌相对血流量,并作为心肌血流灌注定量判断标准。结果 MCE所测定的左心室心肌缺血面积与美蓝染色后缺血面积实际参数高度一致(r=0.93,P=0.01)。回顾分析各个感兴趣点的定量指标,心肌正常灌注区的峰值强度(A)、曲线斜率(β)显著高于缺血区。缺血心肌区灌注量(A.β)较正常心肌区降低约70%,与心肌正常灌注区之间差异有统计学意义(P<0.05)。临界区灌注量(A.β)较正常心肌区降低约50%,与心肌正常灌注区之间差异有统计学意义(P<0.05)。结论 MCE可用于心肌缺血面积的估测,测定心肌缺血范围,确定心肌缺血的临界点。     

经静脉实时心肌造影超声心动图评估心肌梗死后存活心肌

目的探讨经静脉实时心肌造影超声心动图（RT-MCE）评估心肌梗死后存活心肌。方法18例准备进行血运重建术心肌梗死患者,于术前1-5天行RT-MCE检查,并于术后3个月再次行常规超声心动图检查,室壁运动分析采用18节段分析法,分为运动正常、运动减弱、无运动和反常运动。心肌存活定义为术后超声检查室壁运动明显改善。将造影结果分为3种情况：充盈缺损,造影剂充盈延迟、回声稀疏不均匀或心内膜下充盈缺损,回声均匀性增强。其中后两种情况定义为存活心肌。结果在18例心肌梗死患者中共检出109个室壁运动异常节段,运动减弱为47个,无运动为56个,反常运动为6个。注射造影剂后回声均匀性增强的心肌节段中有2个节段术前室壁运动减弱,术后运动均改善;回声不均匀或心内膜下充盈缺损的心肌节段中术前室壁运动减弱有24个节段,术后运动改善14个,术前室壁无运动有24个节段,术后运动改善20个;充盈缺损的心肌节段中术前室壁运动减弱有21个节段,术后运动均未改善,术前室壁无运动32个,术后运动改善2个。RT-MCE检出存活心肌的敏感性、特异性分别为94.7%、78.9%。结论RT-MCE能比较准确的判断心肌梗死后心肌的存活性。     

Acute myocardial infarction in a child with myocardial bridge

BACKGROUND:

Myocardial infarction (MI) is rare in children, and Kawasaki disease is now recognized as the main cause for MI. In this report, we present a child with MI caused by myocardial bridge (MB).

METHODS:

A 7.5-year-old boy was admitted to Weifang People’s Hospital on September 16, 2008 for heart disease. By electrocardiogram, coronary CT angiography, emission computed tomography, and other examinations, he was initially diagnosed as having (1) acute inferior myocardial infarction and extensive anterior myocardial infarction; (2) fulminant myocarditis; or (3) coronary myocardial bridge. He was treated with oxygen, thrombolysis, myocardial nutrition, vitamin C (4.0 g per time), dexamethasone (7.5 mg per time), a large dose of gamma globulin, and interferon.

RESULTS:

Myocardial enzymes, liver function, C-reactive protein, and troponin-I returned to normal at 21 days after treatment. At 29 days, electrocardiogram indicated that II, III, aVF, V4 - V6 leads had abnormal Q wave, and ST-T changed. The patient was discharged.

CONCLUSION:

Myocardial bridge may be one of the causes of MI in children.KEY WORDS: Myocardial bridge, Electrocardiogram, Acute myocardial infarction     

心肌对比超声心动图估测心肌血流量的价值

目的评价心肌对比超声心动图测定心肌血流量的可行性.方法建立急性心肌梗死犬模型,以放射性微球测定的心肌血流量为"金标准”,经外周静脉持续滴注微泡造影剂,通过计算平台声强度(A)和微泡再充填速率(β)测定心肌相对血流量.结果放射性微球法所测的心肌血流量和心肌对比超声心动图测定的A*β值相关良好(r=0.81,P=0.001).结论经静脉持续滴注微泡造影剂行心肌对比超声心动图可估测心肌相对血流量.     

Regional myocardial shape alterations in patients with anterior myocardial infarction

Objective: To assess the impact of regional left ventricular curvature in patients with an acute anterior myocardial infarction on ventricular volume.Methods: Left ventricular curvature was calculated at 100 points from apical four chamber echocardiograms of 68 patients with an acute anterior wall infarction. Curvature at any point of the contour was defined as the reciprocal of the radius of the circle that intersects that point tangentially and was independent of volume and geometric assumptions. Curvature, volume and shape of the patient group was compared with these measurements in 20 normal volunteers.Results: Diastolic curvature differed at the borderzone of the infarct and the apical area. In the basal septal area (point 9–18) mean curvature was lower in the patient group (0.1±2.7 versus 2.1±0.7; p<0.0001) as compared to the normal individuals. In the mid-septal area (point 22 to 27), mean curvature was more concave (? 0.1±2.6) in the patient group corresponding to in the normal population (? 0.4±1.3) p<0.005. In the apex point 52 and 53 diverged with a curvature of 9.9±1.9 in patients versus 9.4±2.9 p<0.005 in normal individuals. Systolic curvature diverged at the basal septum (point 1–4) with a mean curvature of 1.4±1.1 in patients compared to 3.5±2.5 in normal individuals p<0.01. Curvature differed also in the mid-septal region (point 9–29) with a curvature of ? 1.7±1.2 in patients versus 0.4±0.9 (p<0.01) in normal individuals and in the apical septum (point 48–52) with a curvature of 16.6±5.2 in patients and 13.9±2.6 (p<0.0001) in healthy individuals. Separation of patients with the greatest curvature alteration to those with minor curvature change revealed, that baseline curvature analysis can discriminate patients at risk for left ventricular remodelling.Conclusion: Regional curvature analysis correctly identifies the geometric changes induced by myocardial infarction. Apical systolic curvature can distinguish those patients that are at risk for left ventricular remodelling from those who are not at risk.     

组织多普勒成像检测等容收缩期运动评价心肌梗死患者心肌存活性的研究

目的 探讨静息状态下局部心肌等容收缩期运动指标评价陈旧性心肌梗死患者心肌存活性的临床价值.方法 应用组织多普勒成像(TDI)对30例陈旧性心肌梗死患者和30例正常人局部心肌等容收缩期运动系列指标进行检测,于胸骨旁左室长轴观,心尖左室长轴观、两腔观和四腔观,将取样门宽分别置于左室基底段和中段内膜下心肌层,获取16个节段的TDI,测量等容收缩期正、负向波(IVC1,IVC2)峰值速度(V,VIVC2)及其差值(DIVC)等,并与单光子发射计算机断层成像(SPECT)所测心肌存活分数(VF)对比分析,以VF<30%定为梗死区内无存活心肌.结果 与对照组相应部位相比,心肌梗死组梗死部位VIVC1,DIVC减低(P<0.05～0.01),VIVC2及IVC2持续时间(TIVC2)增大(P<0.05);IVC1持续时间(TIVC1)两组差异无统计学意义(P>0.05);非梗死部位与对照组相比变化多不显著(P>0.05);心肌梗死节段横向DIVC明显小于同一节段纵向DIVC,差异有统计学意义(P<0.05).相关分析显示TDI所测心肌横向及纵向DIVC值与SPECT心肌灌注显像所测VF呈显著正相关,相关系数分别为0.837(P<0.001)和0.797(P<0.001).若以横向DIVC>-1.50为截断值预测局部心肌具有存活性的敏感性为75%,特异性达75%;以纵向DIVC值>0.92为截断值预测局部心肌具有存活性的敏感性达77.8%,特异性为87.5%.结论 心肌梗死患者梗死区等容收缩期TDI具有特征性变化,应用横向及纵向DIVC均可作为静息状态下评价心肌存活性的新指标.     

Acute myocardial infarction associated with myocardial bridge and coronary artery vasospasm

A 65-year-old man was admitted to our hospital with acute myocardial infarction (MI). Emergency coronary angiography showed no significant organic lesions, but a myocardial bridge was found at the mid-left anterior descending artery An acetylcholine provocation test revealed 90% spastic stenosis just proximal to the myocardial bridge. His acute MI could have been caused by both a coronary spasm and the myocardial bridge.     

Complications associated with myocardial infarction

The incidence of complications after acute myocardial infarction (MI) has been estimated to range from 14-95 per cent, with an overall one-month mortality of 30 per cent. Early treatment, as advocated by the National Service Framework for Heart Disease, has brought about some reduction in associated morbidity and mortality after MI. This article reviews the common complications associated with an acute MI, such as cardiogenic shock, pericarditis and heart failure. Nurses who are knowledgeable about potential complications should be able to detect early signs and symptoms, initiate emergency treatment, and prevent profound haemodynamic compromise occurring.     

The phenomenon of intermittent myocardial ischemia and characteristics of myocardial reserve in patients with myocardial infarction

AIM: To study coronary and myocardial reserves in myocardial infarction survivors (MIS) with consideration of development of intermittent ischemia during transesophageal pacing (TEP). MATERIAL AND METHODS: 320 MIS were examined 1.5-2 months after myocardial infarction onset. 30 healthy male volunteers served control. Stepwise overdrive TEP was made in all the examinees with parallel estimation of central hemodynamics by tetrapolar chest rheography with assessment of systolic and diastolic parameters. RESULTS: In the course of TEP, 39.4% MIS developed intermittent ischemia (II) at frequencies 120-140 imp/min. II presented as a significantly depressed ST segment on ECG. There was a simultaneous lengthening (1.4-fold) of diastole and a fall (1.5-fold) of end-diastolic pressure in the left ventricle (EDP). At frequencies 140-160 imp/min the length of the diastole shortened while EDP rose. CONCLUSION: The II phenomenon demonstrates a key role of coronary reserve. Changes in coronary and myocardial reserves during TEP in II development are interrelated. They may represent unknown adaptive mechanisms of the myocardium protecting against unfavourable outcomes of ischemic episodes.