快速检测心肌标志物诊断急性心肌梗死的价值

目的探讨快速联合检测肌红蛋白(Myo)、心肌肌钙蛋白I(CTnI)、肌酸激酶同工酶MB(CK-MB)诊断急性心肌梗死(AMI)的价值。方法采用免疫金标法对疑似AMI患者于发病后不同时间进行心肌标志物(Myo、CTnI、CK-MB)的快速检测,并与生化指标心肌酶谱结果进行对照。结果心肌标志物诊断AMI的敏感度为95.8%,特异度为95.1%,均高于心肌酶谱的敏感度(69.9%)和特异度(70.7%)。联合检测Myo、CK-MB、CTnI在保证敏感度的前提下提高了方法的特异度。结论心肌标志物可以取代心肌酶谱对心肌损伤做出诊断,即时检验(POCT)检测系统对于AMI的及时诊断有重大意义。     

新型心肌损伤标志物与传统心肌酶对诊断早期急性心肌梗死的敏感度和特异度评价

目的探讨新型心肌损伤标志物与传统心肌酶对诊断早期急性心肌梗死(AMI)的敏感度及特异度评价。方法选取2013年1月至2015年6月该院有AMI发病指征的疑似210例患者作为研究组,并选择同时间段有胸痛指征疑似AMI但确诊为非AMI的210例患者作为对照组。初诊患者均检测新型心肌损伤标志物心肌钙蛋白(cTnI)、心型脂肪酸结合蛋白(HFABP)、肌红蛋白(MYO)和传统心肌酶谱肌酸磷酸激酶(CK)、肌酸磷酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH),在发病后3h,3~6h,以3h间隔抽取静脉血离心血清。比较两组检测结果。结果研究组0~3h、3~6h的H-FABP、cTnI和MYO水平显著高于对照组,并且逐渐升高,升高幅度明显大于传统心肌酶指标,差异具有统计学意义(P0.05);3~6h的CK-MB、LDH显著高于对照组,差异有统计学意义(P0.05);H-FABP、cTnI、MYO敏感度和特异度均相对高于传统心肌酶指标,差异具有统计学意义(P0.05),其中H-FABP在3~6h的特异度和敏感度均最高。结论传统心肌酶用于排除AMI疑似患者,缺乏敏感度和特异度,可采用连续监测法代替判断AMI。新型心肌损伤标志物用于诊断早期急性心肌梗死,敏感度及特异度均优于传统心肌酶法,值得推广应用。     

人外周血心肌肌钙蛋白Ⅰ基因表达水平与心肌损伤程度的关系

目的:分子生物技术的发展,使监测心肌微小损伤成为可能。探讨外周血心肌肌钙蛋白Ⅰ(cardiactroponinⅠ,cTnⅠ)-mRNA对心肌损伤诊断的临床价值。方法:以电镜观察心肌损伤时的超微结构改变;从心肌组织和外周血中制备总RNA,以随机引物和反转录酶合成cTnⅠ-cDNA,再以巢式PCR扩增和测序分析;将cTnⅠ-mRNA扩增法用于临床诊断,与心肌酶谱(CK,CK-MB,AST,LDH)及cTnⅠ定性比较,以探讨其临床价值。结果:心肌损伤组织超微结构表现为心肌线粒体肿胀、嵴断裂、严重空泡样变及细胞核异形变、染色质浓缩边聚。巢式PCR法扩增cTnⅠ-mRNA片段的灵敏度为2μg/L,测序分析证实从心肌组织及外周血中扩增基因片段与原序列完全一致。对62例慢性心脏病患者外周血cTnⅠ-mRNA的扩增分析,其阳性率明显高于酶谱或cTnⅠ定性分析(P<0.05)。结论:心肌损伤时cTnⅠ-mRNA释放进入外周血,为心肌损伤诊断的敏感基因标志物。     

D-二聚体、cTnT及心肌酶谱检测在急性心肌梗死诊断中的价值

目的探讨D-二聚体(D-D)、肌钙蛋白T(cTnT)及心肌酶谱检测在急性心肌梗死(AMI)临床诊断中的价值。方法选取AMI患者36例(AMI组)和体检健康者20例(健康对照组)作为研究对象,检测两组血浆D-D、cTnT、心肌酶谱水平及其灵敏度、特异度。结果 AMI组D-D、cTnT、肌酸激酶(CK)、肌酸激酶同工酶MB(CK-MB)、天门冬氨酸氨基转移酶(AST)、乳酸脱氢酶(LDH)水平均明显高于健康对照组,差异均有统计学意义(P0.05)。AMI患者中,cTnT、D-D、心肌酶谱的阳性率分别为91.67%、69.44%、66.67%,cTnT阳性率明显高于D-D和心肌酶谱(P0.05)。血浆cTnT对AMI的诊断灵敏度和特异度明显高于D-D和心肌酶谱(P0.05)。结论与D-D和心肌酶谱相比,cTnT对AMI的诊断灵敏度和特异度更好,临床上可多项联合检测提高检测准确性。     

透射免疫比浊法检测CK-MBmass在ACS诊断中的价值

目的评价透射免疫比浊法检测肌酸激酶同工酶质量(CK-MBmass)在急性冠状动脉综合征(ACS)诊断中的应用价值。方法选择69例急性心肌梗死(AMI)患者及69例不稳定型心绞痛(UA)患者为研究对象,采用透射免疫比浊法同时检测两组患者血清中CK-MBmass、心肌肌钙蛋白I(cTNI)、肌红蛋白(MYO)及脂肪酸结合蛋白(FABP),比较组间4项心肌损伤标志物的水平及阳性检出率;应用受试者工作曲线(ROC)评价各项心肌损伤标志物单独及联合检测在ACS中的诊断价值。结果 AMI组的4项心肌损伤标志物水平与检出率均高于UA组,差异均有统计学意义(P0.05);CK-MBmass、cTNI、MYO及FABP对AMI的最佳诊断界限值分别为8.265、0.475、108.875、9.435ng/mL,CK-MBmass的ROC曲线下面积(AUC)、准确度、灵敏度、特异度、Youden指数分别为0.998、0.986、0.971、1.000、0.971,与4项心肌损伤标志物联合检测相似,略高于其他3项标志物。结论透射免疫比浊法检测CK-MBmass对于ACS的临床诊断具有一定价值,可以较好地满足临床需求。     

人外周血心肌肌钙蛋白Ⅰ基因表达水平与心肌损伤程度的关系

目的：分子生物技术的发展，使监测心肌微小损伤成为可能。探讨外周血心肌肌钙蛋白Ⅰ(cardiac troponin Ⅰ，cTnⅠ)-mRNA对心肌损伤诊断的临床价值。方法：以电镜观察心肌损伤时的超微结构改变；从心肌组织和外周血中制备总RNA，以随机引物和反转录酶合成cTn Ⅰ-cDNA，再以巢式PCR扩增和测序分析；将cTn Ⅰ-mRNA扩增法用于临床诊断，与心肌酶谱(CK，CK-MB，AST，LDH)及cTnⅠ定性比较，以探讨其临床价值。结果：心肌损伤组织超微结构表现为心肌线粒体肿胀、嵴断裂、严重空泡样变及细胞核异形变、染色质浓缩边聚。巢式PCR法扩增cTn Ⅰ-mRNA片段的灵敏度为2μg／L测序分析证实从心肌组织及外周血中扩增基因片段与原序列完全一致。对62例慢性心脏病患者外周血cTn Ⅰ-mRNA的扩增分析，其阳性率明显高于酶谱或cTnⅠ定性分析(P&;lt;0．05)。结论：心肌损伤时cTn Ⅰ-mRNA释放进入外周血，为心肌损伤诊断的敏感基因标志物。     

心肌肌钙蛋白Ⅰ检测对急性心肌梗死诊断临床应用价值

目的探讨心肌肌钙蛋白Ⅰ(cTnI)测定对急性心肌梗死(AMI)的诊断价值.方法采用化学发光免疫法测定AMI患者血清cTnI,用全自动化分析仪测定心肌酶学(CK、CK-MB、LDH、AST).结果 cTnI测定敏感性高于心肌酶学测定(P＜0.05).结论 cTnI是一种特异性和敏感性具佳的心肌损伤血清标志物,对AMI的诊断价值高于心肌酶学测定.     

心肌肌钙蛋白Ⅰ对急性心肌梗死的诊断价值

急性心肌梗塞（AMI）的早期诊断对AMI患者的及时救治，减少心肌坏死。防止心脏突发事件，改善预后有重要意义。心肌肌钙蛋白Ⅰ（cTnⅠ）是近年发展起来的一种高敏感、高特异诊断AMI的心肌损伤标志物。为了更好地开展cTnⅠ测定及其在临床心肌损伤疾病诊断中的应用．本文通过对胸痛患者血清cTnⅠ与肌酸激酶同工酶（CK—MB）检测结果进行比较，旨在探讨cTnⅠ对AMI的诊断价值。     

心肌损伤标志物联合检测在急性心肌梗死诊断中的价值

目的评价心肌损伤标志物肌钙蛋白T/I(cTnT/I)、肌红蛋白(Myo)、肌酸激酶同工酶(CK-MB)在急性心肌梗死(AMI)中的诊断价值。方法对150例AMI患者进行心肌标志物和心肌酶谱比较。结果心肌标志物在AMI发病早期升高的幅度较心肌酶谱升高显著,差异有统计学意义(P0.01)。结论心肌损伤标志物cT-nT/I、Myo、CK-MB在AMI早期诊断中具有重要的临床价值。     

hs-cTnⅠ和常规心肌标志物早期诊断微小心肌损伤的临床价值

目的分析高敏肌钙蛋白I(hs-cTnⅠ)和常规心肌标志物早期诊断微小心肌损伤的临床价值。方法选取77例微小心肌损伤患者为研究组,同期健康体检者77例为对照组。全部入选对象均检测血清hs-cTnⅠ与常规心肌标志物水平,分析两组检测结果。结果研究组hs-cTnⅠ与心肌标志物的检测阳性率均高于对照组(P0.05),研究组中胸痛发作时间3 h者各项指标均低于3~6 h者(P0.05),胸痛发作时间于3 h者各项指标水平高于对照组(P0.05)。结论在微小心肌损伤患者的早期诊断中,检测hs-c TnⅠ和常规心肌标志物,可提高心肌损伤确诊率。     

心肌超声造影评价兔心肌梗死与存活性

目的探讨心肌超声造影（myocardial contrast enhancement,MCE）评价兔心肌梗死及心肌存活的价值。方法采用冠状动脉左前降支（left anterior descending of coronary artery,LAD）结扎法建立兔心肌梗死模型。建模1周后心肌超声造影,左室乳头肌短轴观显示局部心肌血流灌注情况。梗死区心肌组织行Masson三色染色后与MCE进行对照。结果MCE显示模型兔左室前壁、前间隔灌注缺损与灌注不良或延迟的节段数分别为18、14,与邻近正常灌注区灰阶值比较,差异有十分显著的统计学意义（P〈0.05）。与病理染色判断梗死与存活节段对比,MCE预测心肌梗死的敏感性、特异性、阳性预测值分别为88.2%、80%和83.3%,对心肌存活的敏感性、特异性及阳性预测值分别为80%、88.2%和85.7%。结论MCE判断兔心肌梗死与心肌存活的敏感性、特异性及准确性较高。     

冠状动脉心肌桥与心肌缺血关系的研究

目的：探讨心肌桥（MB）与心肌缺血的关系。方法：回顾分析冠脉造影中检出的88例MB患者,把其中36例孤立性MB分为两组（A组：NobleI级;B组：NobleⅡ～Ⅲ级）,卡方检验分析：（1）壁冠状动脉及其前后冠脉的粥样硬化发生率差异;（2）A、B组的动态心电图的ST—T段改变发生率、运动平板阳性率、稳定性心绞痛发生率、不稳定性心绞痛发生率的差异。结果：MB检出率4．1％,B组与A组相比,运动平板阳性率、稳定性心绞痛发生率、不稳定性心绞痛发生率明显升高（P〈0．05）;MB近段冠脉的AS发生率高于壁冠状动脉及MB远段冠脉（P〈0．01）。结论：MB的狭窄程度越严重,引起的心肌缺血越重;MB促进近段冠脉粥样硬化的发生。     

家兔实验性心肌梗塞时心肌细胞凋亡研究

目的：探讨急性心肌梗塞时心肌细胞凋亡情况。方法：采用ＤＮＡ缺口末端标记法（ＮＥＬＭ）、透射电镜和琼脂糖凝胶电泳对家兔实验性心肌梗塞时不同损伤区心肌细胞凋亡情况进行研究。结果：在梗塞交界区心肌组织中可见散在大量ＭＥＬＭ染色阳性细胞；电镜检查细胞呈凋亡特征。在坏死区和正常心肌组织中均未发现ＮＥＬＭ染色阳性细胞。梗塞交界区ＤＮＡ电泳呈梯状，符合细胞凋亡图谱。坏死区心肌ＤＮＡ电泳图谱呈均匀弥散状态，正常心     

实时心肌造影超声心动图再充盈参数评估心肌梗死后心肌存活性

目的 探讨实时心肌造影超声心动图(myocardial contrast echocardiography,RT-MCE)评价血运重建术前心肌灌注情况和再充盈参数评估心肌梗死后心肌存活性.方法 18例准备进行血运重建术心肌梗死患者,于术前1～5 d行RT-MCE检查,并于术后3个月再次进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3个月超声检查室壁运动明显改善.分析造影图像,根据灌注的函数公式Y(t)=A[1-e-kt] B,得出A值、k值、A×k值.利用接受者操作特征(receiver operator characteristics,ROC)曲线定义RT-MCE再充盈参数预测心肌梗死后心肌存活性的截断值以及敏感性、特异性.结果 (1)在18例患者中共109个室壁发生明显运动异常,运动减弱为47个,无运动为56个,反常运动为6个,术后3个月室壁运动改善分别为16个,22个,0个;(2)术后3个月室壁运动改善节段的术前心肌造影各参数A值、k值、AXk值[分别为(5.48±1. 73)dB、(0.34±0.09)S-1、(2.12±1.71)dB/s],明显大于3个月功能未恢复心肌的A值、k值、A×k值[分别为(4.41±1.45)dB、(0.26±0.06)S-1、(1.15±0.76)dB/s],差异有统计学意义(P均＜0.01);(3)以术前A值＞3.75 dB为截断值预计心肌存活性的敏感性为80.0%,特异性为79.2%,以术前k值＞0.28 S-1预计心肌存活性的敏感性为85.0%,特异性为81.1%,以术前A×k值＞1.32 dB/s预计心肌存活性的敏感性为85.0%,特异性为84.9%. 结论 RT-MCE再充盈参数可以较准确地检测心肌梗死后室壁运动异常节段的心肌灌注情况,评价心肌梗死后心肌存活性.     

Determinants of Myocardial Strain in Experimental Chronic Myocardial Infarction

We evaluated the relationships between regional myocardial strain measured by speckle tracking echocardiography and viability, fibrosis, hypertrophy and oxygen consumption in the infarcted or remote myocardium in a pig model of chronic myocardial infarction (MI). Thirteen farm pigs with surgical occlusion of the left anterior descending coronary artery and five sham-operated pigs were studied 3 mo post-MI. Computed tomography revealed significant left ventricle remodeling. Reduced radial or circumferential strain identified areas of transmural infarction (area under the curve: 0.82 and 0.79, respectively). In the remote non-infarcted area, radial strain correlated inversely with the amount of fibrosis (r?=?–0.66, p?=?0.04) and myocyte hypertrophy (r?=?–0.68, p?=?0.03). Radial strain rate inversely correlated with myocardial resting oxygen consumption assessed with ¹¹C-labeled acetate positron emission tomography (r?=?–0.71, p?=?0.006). In conclusion, myocardial strain and strain rate reflect fibrosis, hypertrophy and oxygen consumption of the remote areas after MI.     

声学密度定量技术在急性心肌梗塞早期预测再灌注心肌的存活

目的：本试验是利用声学密度定量技术（ＡＤ－ＩＢＳ）预测再灌注心肌存活。方法：在发病当天,发病后第３天,第２１天分别对２０例急性心肌梗塞患者进行ＡＤ－ＩＢＳ检查。结果：标化ＣＶＩＢ在发病后第３天有所恢复（不依赖于室壁运动的恢复）的梗塞区心肌,其在发病后第２１天的室壁增厚率可达到与正常心肌区无明显差异。结论：帮可认为心肌梗塞后标化ＣＶＩＢ可早期预测再灌注心肌的存活。     

Evaluation of Myocardial Stiffness in Hypertensive Patients by Intrinsic Wave Propagation of the Myocardial Stretch

The objective of the study was to evaluate myocardial stiffness in hypertensive patients by measuring the intrinsic velocity propagation (IVP) of the myocardial stretch and to explore the correlation between IVP and cardiac systolic and diastolic functions. Eighty-one hypertensive patients and 53 healthy patients were prospectively enrolled in this study. IVP was measured using high-frame rate tissue Doppler (350−450 frames per second). IVP was significantly higher in hypertensive patients than in the control group (1.53 ± 0.39 m/s vs. 1.40 ± 0.19 m/s, p = 0.031). In the hypertensive group, IVP was significantly higher in patients with electrocardiogram (ECG) strain than in those without ECG strain (1.63 ± 0.46 m/s vs. 1.45 ± 0.32 m/s, p = 0.047). Moreover, IVP exhibited a good correlation with interventricular septal thickness at end-diastole (r = 0.434, p < 0.001), left ventricular posterior wall thickness at end-diastole (r = 0.439, p < 0.001), E/A ratio (r = 0.245, p = 0.004) and global longitudinal systolic strain (r = 0.405, p < 0.001). IVP was significantly higher in hypertensive patients, which indicates elevated myocardial stiffness in this cohort of patients. This novel measurement exhibited great potential for use in clinical practice to assess myocardial stiffness in patients with hypertension non-invasively.     

Myocardial Injury Induced by Ultrasound-Targeted Microbubble Destruction: Evidence for the Contribution of Myocardial Ischemia

Ultrasound-targeted microbubble destruction (UTMD) can cause left ventricular (LV) dysfunction and tissue alterations in rats when high ultrasound (US) energy and long duration of imaging are used. However, the mechanism underlying these alterations remains unclear. The aim of the present work was to investigate the possible role of ischemia in the pathogenesis of the UTMD-induced LV damages in rats. To address this issue, rat hearts were exposed in situ to perfluorocarbon-enhanced sonicated dextrose albumin (PESDA) and US at peak negative pressures of 0.6, 1.2 or 1.8 MPa for 1, 3, 9, 15 or 30 min. Blood pressure and electrocardiogram were continuously recorded during insonation. LV function was assessed before and immediately after US exposure, as well as at 24 h and 7 d. At each time point, groups of rats were euthanized and their hearts were harvested for morphologic analysis. Rats exposed to either PESDA alone or US alone showed no functional or morphologic abnormalities. By contrast, rats exposed to both PESDA and US exhibited transient LV dysfunction, transient ST-segment elevation, premature ventricular contractions, microvascular ruptures, contraction band necrosis and morphologic tissue damage. These bio-effects were spontaneously and completely reversible by one week, except in the groups exposed to the highest peak negative pressure for the longest duration, in which mild dysfunction persisted and interstitial fibrosis developed. In conclusion, simultaneous exposure of rat hearts to PESDA and US in vivo results in significant bio-effects that are similar to myocardial ischemia, including transient regional LV dysfunction, transient ST-segment elevation and myocyte contraction band necrosis. (E-mail: vanoverschelde@card.ucl.ac.be)