实验性顿抑心肌的微循环障碍

为了探讨顿抑心肌微循环改变及机制，制备左前降支冠状动脉不同阻断时间(15min和60min)后再灌注犬心肌顿抑模型，在不同观察时间点静脉注射舍全氟丙烷声振白蛋白微泡造影剂，采用二次谐波成像和间歇发射技术行心肌声学造影，计算心肌声学造影图像上心肌视频密度峰值、心肌声学造影曲线上升斜率和曲线早期下降斜率，测定相应时间点冠状静脉窦血乳酸浓度，结果发现，心肌顿抑早期心肌视频密度峰值显著增高，1h后恢复至结扎前水平；再灌注期顿抑区与正常区视频密度峰值比值、心肌声学造影曲线上升斜率比值、心肌声学造影曲线早期下降斜率比值显著高于左前降支冠状动脉结扎前，随着再灌注时间的延长比值逐渐回降；再灌注期冠状静脉窦血乳酸浓度明显增高。以上结果提示，心肌顿抑早期心肌微循环处于“高动力”状态，血流灌注增加与排空加快并存；顿抑心肌缺氧代谢加强；心肌内微循环短路可能是心肌顿抑微循环障碍的机制。     

实验性顿抑心肌微血管结构和功能改变

目的 探讨心肌顿抑时心肌微血管结构和功能改变。方法 制备冠状动脉左前降支（LAD）不同阻断时间（15min和60min)后再灌注犬心肌顿抑模型，在不同观察时间点静脉注射含全氟丙烷声振白蛋白微泡造影剂，采用二次谐波成像和间歇发射技术行心肌声学造影。由主动脉根部分别注射乙酰胆碱（ACH）和硝酸甘油（NG）后重复心肌声学造影，并计算用药后／前二维超声上所示心肌灰阶峰值比值（PVIR）和顿抑区与正常区心肌灰阶峰值比值的比值PVIRR。心肌标本行透射电镜检查。结果 （1）LAD阻断15min组再灌注早期NG－PVIR和ACH－PVIR明显减低，但分别在再灌注60min和120min时恢复至结扎前水平；（2）LAD阻断60min组再灌注早期NG－PVIR减低，至再灌注120min时才恢复到结扎前水平，而再灌注ACH-PVIR明显减低，随着再灌注时间的延长虽有逐渐回升趋势，但至再灌注120min仍未恢复至结扎前水平；（3）两组PVIRR的变化与PVIR一致，唯恢复稍慢；（4）LAD阻断15min组心肌毛细血管和内皮细胞结构未见明显改变，而LAD阻断60min组毛细血管内皮细胞肿胀，内皮细胞间连接间隙稍增宽。结论 顿抑心肌微血管舒张功能受损，缺血时间较长则还有微血管结构改变，其受损的细胞主要是内皮细胞。     

心肌顿抑中的氧化应激作用及氨基胍干预的效果

背景氧化应激的超氧阴离子(O-·2)可与细胞一氧化氮合酶(NOS)释出的一氧化氮(NO)结合,生成过氧亚硝酸阴离子(ONOO-).ONOO-是氧化应激各种产物[如O-·2、H2O2、羟自由基(·OH)等]之一,统称为反应性氧族(ROS).ROS在心肌顿抑中的作用研究不多,氨基胍作为NOS抑制剂对ROS的作用也不清楚.目的 探讨ONOO-在心肌顿抑发生中的作用和机制以及氨基胍的干预作用.方法 24条雄性杂种犬,随机分为4组:1)短顿抑组[左前降支冠状动脉(LAD)阻断15 min/再灌注120 min];2)长顿抑组(LAD阻断60 min/再灌注120 min);3)氨基胍组[LAD阻断60 min/再灌注120 min加一氧化氮合酶抑制剂氨基胍(100 mg/kg)干预];4)假手术组.在不同观察时间点测定超声心功能和冠状静脉窦血浆NO浓度.实验完毕后心肌标本行电镜检查,并行硝基酪氨酸免疫组化检查以证实是否有ONOO-生成.结果 1)LAD结扎后缺血心肌节段收缩期增厚百分率和左室射血分数显著下降,缺血心肌节段表现为矛盾运动;再灌注开始后心肌节段收缩功能和左室射血分数呈进行性改善,短顿抑组和氨基胍组心功能的恢复快于长顿抑组.2)短顿抑组和长顿抑组再灌注期血浆NO浓度明显升高,氨基胍组再灌注期血浆NO浓度无显著升高.3)短顿抑组顿抑心肌硝基酪氨酸免疫组化染色见阳性染色的心肌细胞灶;长顿抑组见较大、较多的强阳性染色心肌细胞灶,主要是胞浆尤其横纹处染色较深;氨基胍组顿抑心肌偶见心肌细胞弱阳性染色.4)透射电镜观察发现,短顿抑组心肌细胞偶见线粒体轻度脱颗粒;长顿抑组心肌细胞部分肌丝断裂,收缩带溶解,线粒体肿胀、脱颗粒,胞质水肿;氨基胍组心肌超微结构保存良好.结论 1)顿抑心肌生成NO增多伴ONOO-形成;2)ONOO-主要攻击的蛋白质对象是肌丝上的蛋白质;3)氨基胍抑制顿抑心肌过多的NO生成,显著减少ONOO-形成,并对顿抑心肌的超微结构和功能有明显保护作用.     

心肌顿抑中的氧化应激作用及氨基胍干预的效果

背景氧化应激的超氧阴离子(O-.2)可与细胞一氧化氮合酶(NOS)释出的一氧化氮(NO)结合,生成过氧亚硝酸阴离子(ONOO-)。ONOO-是氧化应激各种产物[如O2.-、H2O2、羟自由基(.OH)等]之一,统称为反应性氧族(ROS)。ROS在心肌顿抑中的作用研究不多,氨基胍作为NOS抑制剂对ROS的作用也不清楚。目的探讨ONOO-在心肌顿抑发生中的作用和机制以及氨基胍的干预作用。方法24条雄性杂种犬,随机分为4组:1)短顿抑组[左前降支冠状动脉(LAD)阻断15min/再灌注120min];2)长顿抑组(LAD阻断60min/再灌注120min);3)氨基胍组[LAD阻断60min/再灌注120min加一氧化氮合酶抑制剂氨基胍(100mg/kg)干预];4)假手术组。在不同观察时间点测定超声心功能和冠状静脉窦血浆NO浓度。实验完毕后心肌标本行电镜检查,并行硝基酪氨酸免疫组化检查以证实是否有ONOO-生成。结果1)LAD结扎后缺血心肌节段收缩期增厚百分率和左室射血分数显著下降,缺血心肌节段表现为矛盾运动;再灌注开始后心肌节段收缩功能和左室射血分数呈进行性改善,短顿抑组和氨基胍组心功能的恢复快于长顿抑组。2)短顿抑组和长顿抑组再灌注期血浆NO浓度明显升高,氨基胍组再灌注期血浆NO浓度无显著升高。3)短顿抑组顿抑心肌硝基酪氨酸免疫组化染色见阳性染色的心肌细胞灶;长顿抑组见较大、较多的强阳性染色心肌细胞灶,主要是胞浆尤其横纹处染色较深;氨基胍组顿抑心肌偶见心肌细胞弱阳性染色。4)透射电镜观察发现,短顿抑组心肌细胞偶见线粒体轻度脱颗粒;长顿抑组心肌细胞部分肌丝断裂,收缩带溶解,线粒体肿胀、脱颗粒,胞质水肿;氨基胍组心肌超微结构保存良好。结论1)顿抑心肌生成NO增多伴ONOO-形成;2)ONOO-主要攻击的蛋白质对象是肌丝上的蛋白质;3)氨基胍抑制顿抑心肌过多的NO生成,显著减少ONOO-形成,并对顿抑心肌的超微结构和功能有明显保护作用。     

计算机辅助心肌造影负荷超声定量评价心肌灌注及局部收缩功能

目的 探讨计算机辅助心肌造影负荷超声(MCSE)定量评价心肌灌注和局部收缩功能的应用价值.方法 采用急性阻断再灌注左室支建立兔模型,根据阻断和再灌注时间分为两组:阻断30 min后再灌注60 min(Ⅰ组)和阻断120 min后再灌注60 min(Ⅱ组).分别在基础状态、阻断、再灌注和多巴酚丁胺负荷(5、10、15和20 μg·kg-1·min-1)行心肌造影超声心动图,造影图像经自制计算机辅助软件处理后,自动标出每个节段的标化造影剂密度(CI),根据标化CI值,彩色编码标记为:0～ -20像素(pix)黄色、-21～ -40 pix蓝色、-41～ -70 pix绿色以及＜-70 pix红色.分别计算出阻断时和再灌注后红色编码区面积,并与荧光微球染色和氯化三苯基四氮唑染色面积对照分析.同时测量各阶段危险心肌的收缩期室壁增厚率(WT).结果 (1)阻断时,危险心肌的WT降到零点或呈负值,CI明显低于基础状态,红色编码区面积与荧光染色危险心肌面积呈正相关(r=0.91,P＜0.01).(2)再灌注和多巴酚丁胺5μg·kg-1·min-1后,各组危险心肌的WT和标化CI仍减低.以标化CI-70 pix为截断值,识别梗死节段的敏感性为95%,特异性为87%.红色编码面积与氯化三苯基四氮唑染色梗死心肌面积呈正相关(r=0.89,P＜0.01).(3)随着多巴酚丁胺剂量的增加,Ⅰ组的标化CI恢复至基础状态,WT逐渐增加超过基础水平,但Ⅱ组仍保持较低水平.结论 计算机辅助心肌造影负荷超声可以定量评价心肌灌注和局部收缩功能,是识别顿抑和梗死心肌安全可行的方法.     

一氧化氮对犬心肌顿抑心功能的影响

目的探讨心肌顿抑(myocardialstunning,MS)时局部组织一氧化氮(NO)含量的变化,及补充或抑制NO对顿抑心肌功能的影响.方法将35条犬随机分为5组(每组7条),即MS组、亚硝基左旋精氨酸甲酯(NG-nitro-L-argininemethylester,L-NAME)组、左旋精氨酸(L-Arginine,L-Arg)组、3-morpholinosydnonimine(Sir-1,一种NO供体)再灌注组及对照组.实验组均通过开胸阻断左冠状动脉前降支(LAD)15min再灌注3h建立MS模型,采用微电极法和Greiss法检测心肌表面及冠状窦血中NO含量变化,根据血流动力学监测及经食管彩色多普勒血流仪(transesophagealechocardiography,TEE)观察心功能及缺血节段室壁运动的变化.结果(1)阻断犬LAD15min后,所有犬均发生MS,主要表现为前壁室壁运动减弱,左室±dp/dt减低;(2)缺血再灌注期,顿抑心肌合成NO减少,L-Arg及Sin-1可明显增加顿抑组织的NO含量,而L-NAME则降低NO含量;(3)再灌注L-Arg及Sin-1在早期即可明显减轻顿抑心肌的室壁运动障碍,使心功能相对改善.结论心肌顿抑时局部顿抑组织NO含量减低,再灌注早期补充NO供体Sin-1及前体L-Arg可明显改善顿抑心肌的缩舒功能,而用L-NAME阻断NO的合成后则无此作用.     

云芝多糖防止缺血再灌注心肌早期损伤

为了探讨云芝多糖对心肌缺血再灌注损伤的预防作用，制备犬心肌缺血再灌注损伤模型，输血再灌注组不用药物干预，云芝多糖组手术前2天每天口服云芝多糖150mg/kg。在缺血再灌注过程不同时间点测定左心室舒张压，超声心功能和冠状静脉窦血浆丙二醛浓度，心肌标本行透射电镜检查。结果发现，缺血再灌注组再灌注前和再灌注早期左心室舒张压显著升高，云芝多糖组仅再灌注前左心室舒张压升高，再灌注前两组缺血心肌节段收缩期增厚百分率显著下降，并表现为矛盾运动，再灌注期两组缺血心肌节段收缩期增厚百分率呈进行性改善，至再灌注120min两组均未恢复至结扎前水平，且云芝多糖组显著高于相应时间咪缺血再灌注组；左心室射血分数的变化趋势与缺血心肌节段收缩期增厚百分率相似，但恢复较快，云芝多糖组于再灌注90min即恢复至结扎前水平。缺血再灌注组再灌注期丙二醛浓度明显升高，至再灌注120min尚未恢复至结扎前水平。而云芝多糖组再灌注早期丙二醛浓度升高，但回降较快，于再灌注30min即恢复至结扎前水平，缺血再灌注组心肌组织水肿，心肌细胞少部分肌丝断裂，收缩带模糊，线粒体轻度肿胀，脱颗粒，胞质水肿；云芝多糖组心肌组织除轻微水肿外，未见其它明显结构改变，结果提示，云芝多糖对缺血再灌注早期心肌有显著保护作用。     

丙酮酸对顿抑心肌功能及能量代谢的作用

目的　了解丙酮酸对顿抑心肌功能及能量代谢的影响 ,并分析其可能机制。方法　结扎家兔左冠状动脉前降支 2 0min后 ,再灌注 6h造成短暂缺血 再灌注心肌顿抑模型 ,观察血流动力学、抗氧化酶、脂质过氧化物、血清游离脂肪酸 (FFA)、乳酸 (LD)以及心肌组织的ATP含量和超微结构变化。结果　与顿抑组比较 ,丙酮酸可明显缓解缺血及再灌后心肌功能的损害 ,抑制血清FFA、LD水平的升高 ,降低MDA含量 ,提高SOD活性 ,抑制心肌组织ATP含量降低 ;电镜所见心肌损伤明显比顿抑组轻。丙酮酸组与对照组比较 ,各指标均为显著性差异。结论　丙酮酸可以减少心肌细胞能量消耗 ,保护线粒体的结构和功能 ,对顿抑心肌具有一定保护作用     

心肌顿抑的心电学标志

１　心肌顿抑的概念和分类１９８２年,Ｂｒａｕｎｗａｌｄ及Ｋｌｏｎｅｒ［１］提出了心肌顿抑（ｍｙｏｃａｒｄｉａｌｓｔｕｎｎｉｎｇ）的概念,系指短时间的心肌缺血不发生坏死,但引起的结构、代谢和功能改变在再灌注后需数小时,数天或数周才能恢复正常,顿抑心肌恢复功能所需要的时间依缺血时间长短而异。这种再灌注挽救的但处于缓慢功能恢复的存活心肌称顿抑心肌。其特点是：（１）发生于可逆性缺血（２～２０分钟）再灌注后;（２）心功能障碍是完全可逆,可完全恢复;（３）局部血流正常或几乎正常;（４）局部高能磷酸盐储备降低…     

心肌再灌注损伤与抗氧化剂治疗

<正> 冠脉血流的早期恢复对挽救缺血心肌是至关重要的.但经实验研究已证实,再灌注能引起大量的自由基释放、心肌收缩力损害、再灌注心律失常、细胞死亡.因此,及早应用抗氧化剂治疗,有利于降低再灌注损伤.一、心肌再灌注损伤1.再灌注心律失常 急性缺血血流恢复后观察到的室性心律失常是再灌注损伤的表现,如室性早搏、室颤.再灌注心律失常的发生可能与再灌注后自由基大量产生及钙超载有关.其发生率能被一些抗氧化剂缓解.2.心肌顿抑 心肌再灌注后短暂的机械功能障碍称心肌顿抑,心肌顿抑的发生也与氧自由基及钙失衡有关.目前已证实,心肌顿抑与超氧阴离子自由基、羟基自由基有关,给予抗氧化酶(超氧化物歧化酶SOD、过氧化氢酶CAT)能有效地促进功能恢复,缓解心肌顿抑.     

Detection of recent myocardial ischaemia by molecular imaging of P-selectin with targeted contrast echocardiography.

AIMS: We hypothesized that molecular imaging of endothelial P-selectin expression with targeted myocardial contrast echocardiography (MCE) could identify recently ischaemic myocardium without infarction. METHODS AND RESULTS: The microvascular behaviour of P-selectin-targeted (MB(p)) and control (MB(c)) microbubbles was assessed by intravital microscopy of the cremaster muscle in mice. Targeted MCE imaging with MB(p) and MB(c) was performed in mice after brief left anterior descending (LAD) occlusion and reperfusion and in open- and closed-chest controls. Regional wall motion and perfusion by MCE were assessed during occlusion and after reperfusion. On intravital microscopy, ischaemia-reperfusion produced a 10-fold increase (P < 0.01) in venular attachment for MB(p). Attachment for MB(c) was rare. With myocardial ischaemia-reperfusion, LAD occlusion produced hypoperfusion and wall motion abnormalities that resolved after 45 min of reperfusion. At 45 min, signal enhancement in the post-ischaemic region was four-fold greater (P < 0.05) for MB(p) vs. MB(c). MB(p) produced low-level enhancement in non-ischaemic myocardium in all open-chest animals, suggesting P-selectin expression from surgical cardiac exposure. CONCLUSION: Molecular imaging of P-selectin with targeted MCE can identify the presence of recently ischaemic myocardium in the absence of necrosis and after resolution of hypoperfusion and post-ischaemic stunning. This technique can potentially provide a method for risk stratifying patients with acute chest pain.     

Detection of viable myocardium by transvenous myocardial contrast echocardiography using harmonic power Doppler: canine model of acute coronary occlusion and reperfusion

STUDY OBJECTIVE: To assess whether myocardial contrast echocardiography (MCE) using harmonic power Doppler (HPD) in conjunction with the transvenous contrast agent SHU 563A would be useful in detecting stunned but viable myocardium. DESIGN: Acute coronary occlusion (2 to 3 h) followed by 1 h of reperfusion was created in 10 dogs in an open-chest model. Measurements and results: Continuous harmonic B-mode for wall motion analysis and ECG triggered HPD for assessment of myocardial perfusion was employed during coronary occlusion and after reperfusion. Postmortem 2,3,5-triphenyltetrazolium chloride (TTC) staining was performed to verify infarction. Extent of wall motion abnormality (WMA), perfusion defect size, and anatomic infarct size (myocardial infarction [MI]) were analyzed in a 5-segment model. All 10 dogs showed WMA in 23 of 50 segments during coronary occlusion. In eight dogs, HPD detected perfusion defects in 18 of 50 segments. The concordance rate between WMA and perfusion defect was 86%. Mean linearized power (MLP) in segments with WMA was significantly lower compared to normal segments (60.7 +/- 38.9 vs 110.5 +/- 108.8, p < 0.05). After reperfusion, the extent of WMA was larger than the area of perfusion defect (percentage of left ventricular slice area): 30 +/- 13% vs 9 +/- 8%, p < 0.01. Eventual infarct size was 6 +/- 7%. WMAs were seen in 18 of 50 segments. TTC confirmed MI in 7 of 18 segments. MLP in segments with WMA but no MI was significantly higher compared to segments with WMA and MI (84.5 +/- 67.3 vs 13.2 +/- 9.6, p < 0.01). Thus, the extent of WMA after reperfusion was greater than the size of perfusion defect and eventual MI, indicating the presence of stunned but viable myocardium. CONCLUSION: MCE using HPD and the contrast agent SHU 563A can demonstrate the efficacy of reperfusion, identify necrotic regions, and aid in the recognition of stunned but viable myocardium. This approach could be useful clinically in patients with acute MI undergoing reperfusion therapy.     

Visualization of risk-area myocardium as a high-intensity,hyperenhanced "hot spot" by myocardial contrast echocardiography following coronary reperfusion: quantitative analysis

OBJECTIVES: We examined whether delayed post-injection imaging of a new ultrasound contrast agent (BR-14) could produce prolonged opacification and hyperenhancement of myocardium subjected to coronary occlusion/reperfusion. BACKGROUND: We hypothesized that ultrasound exposure destroyed BR-14 and eliminated visualization of sustained myocardial opacification from retained microbubbles. METHODS: We studied eight open-chest dogs with 3 h of left anterior descending coronary artery (LAD) occlusion followed by 3 h of reperfusion. Myocardial contrast echocardiography (MCE) was performed before occlusion and 120 min after the onset of both occlusion and reperfusion. Ultrasound imaging was initiated 15 min after injection. Myocardial blood flow (MBF) was assessed by microspheres. RESULTS: Pre-occlusion images revealed uniform opacification of left ventricular myocardium greater than that of the cavity, with a mean intensity of the LAD bed of 8.66 +/- 1.38 dB. During occlusion, MCE resulted in the appearance of a perfusion defect in the LAD risk area (intensity 2.08 +/- 1.10 dB). After 120 min of reperfusion, the LAD risk-area myocardium manifested dense opacification of a higher intensity ("hot spot") than baseline (13.7 vs. 8.7 dB), but with reduced MBF consistent with accumulation of a high concentration of microbubbles. Increased MCE intensity was associated with a greater myeloperoxidase score. CONCLUSIONS: These data establish that contrast opacification by BR-14 may be selectively retained within the perfusion bed of a coronary artery subjected to occlusion/reperfusion. Such opacification exhibits defects with occlusion, manifests hyperenhanced intensity (hot spot) with reperfusion, is associated with the level of myeloperoxidase activity, and conforms to the area of myocardium subjected to altered flow.     

Full-motion pulse inversion power Doppler contrast echocardiography differentiates stunning from necrosis and predicts recovery of left ventricular function after acute myocardial infarction.

OBJECTIVES: The goal of this study was to determine, in patients with a recent myocardial infarction (MI) and residual wall motion abnormalities within the distribution of the infarct-related artery, whether normal perfusion by myocardial contrast echocardiography (MCE) would accurately predict recovery of segmental left ventricular (LV) function. BACKGROUND: Left ventricular dysfunction after acute MI may be secondary to myocardial stunning or necrosis. Recent technical innovations in contrast echocardiography, including pulse inversion imaging and power Doppler, now allow full-motion echocardiographic perfusion assessment from a venous injection of fluorocarbon-based contrast agent. METHODS: Thirty-four patients with recent MI underwent baseline wall motion assessment and MCE two days after admission and follow-up echocardiography a mean of 55 days later. RESULTS: Perfusion by MCE predicted recovery of segmental function with a sensitivity of 77%, specificity of 83%, positive predictive value of 90% and overall accuracy of 79%. The mean wall motion score at follow-up was significantly better in perfused, compared with nonperfused, segments (1.4 vs. 2.2, p < 0.0001). Additionally, 90% of perfused segments improved, while the majority of nonperfused segments remained unchanged. CONCLUSIONS: Full-motion MCE utilizing an intravenous fluorocarbon-based agent and pulse inversion power Doppler techniques, identifies stunned myocardium, and accurately predicts recovery of segmental LV function in patients with recent MI.     

Myocardial perfusion echocardiography and coronary microvascular dysfunction

Our understanding of coronary syndromes has evolved in the last two decades out of the obstructive atherosclerosis of epicardial coronary arteries paradigm to include anatomo-functional abnormalities of coronary microcirculation. No current diagnostic technique allows direct visualization of coronary microcirculation, but functional assessments of this circulation are possible. This represents a challenge in cardiology. Myocardial contrast echocardiography (MCE) was a breakthrough in echocardiography several years ago that claimed the capability to detect myocardial perfusion abnormalities and quantify coronary blood flow. Research demonstrated that the integration of quantitative MCE and fractional flow reserve improved the definition of ischemic burden and the relative contribution of collaterals in non-critical coronary stenosis. MCE identified no-reflow and low-flow within and around myocardial infarction, respectively, and predicted the potential functional recovery of stunned myocardium using appropriate interventions. MCE exhibited diagnostic performances that were comparable to positron emission tomography in microvascular reserve and microvascular dysfunction in angina patients. Overall, MCE improved echocardiographic evaluations of ischemic heart disease in daily clinical practice, but the approval of regulatory authorities is lacking.     

静脉心肌声学造影在心肌梗死再灌注治疗及血管成形术中的应用

目的 :探讨静脉心肌声学造影 (MCE)评估急性心肌梗死再灌注治疗效果、冠状动脉介入治疗疗效以及预测存活心肌的价值。方法 :采用HP 5 5 0 0型超声心动仪 ,综合应用二次谐波、间歇成像和能量多普勒成像并采用高能量的超声波发射 ,对3 5例患者静脉注射利声显行MCE ,并行冠状动脉造影进行对比研究。结果 :3 5例患者完成MCE。 17例急性心肌梗死 (AMI)患者中 ,再灌注治疗患者MCE图象评分与保守治疗患者之间差异有显著性 (P <0 0 5 ) ;19例心肌梗死患者行介入治疗 ,共 63个血管重建术相关的心肌节段 ,在心肌梗死急性期 ,介入治疗前MCE显示心肌有灌注 ( 1分或 0 5分 )的心肌节段存活性及术后灌注改善的可能性显著高于MCE无灌注 ( 0分 )的心肌节段 (P <0 0 5 ) ,在心肌梗死陈旧期 ,介入治疗前MCE显示心肌灌注良好 ( 1分 )的心肌节段的存活性及术后灌注改善的可能性显著高于MCE灌注不佳 ( 0分或 0 5分 )的心肌节段 (P <0 0 5 )。结论 :结合多种成像技术 ,利声显可行静脉MCE。MCE可以评估AMI再灌注治疗的疗效 ,评估介入治疗的疗效并判断心肌存活性。     

Detection of Viability of Dysfunctional Myocardium in Coronary Heart Disease. II. Echocardiography

The detection of viable myocardium in patients with severe left ventricular (LV) dysfunction is important because these patients benefit most from revascularization. Three echocardiographic techniques can be used for the noninvasive assessment of functional correlates of viable myocardium. Two-dimensional echocardiography (2DE) is well suited for quantifying resting LV regional and global systolic function and dysfunction before and after revascularization, in addition to providing data on chamber size, shape, and wall thicknesses. The presence of hypokinesis on a resting 2DE indicates that viable myocardium is definitely present, but presence of dykinesis does not exclude viability. Dobutamine stress echocardiography (DSE) before revascularization unmasks viability by demonstrating augmentation of systolic function. Several clinical studies have shown that improvement of regional function during DSE indicates contractile reserve and predicts improvement of function after revascularization. A biphasic response on DSE appears to predict residual coronary artery stenosis and is a reliable marker of viability. DSE also appears to be useful after revascularization for unmasking contractile reserve. Myocardial contrast echocardiography (MCE) detects viability by defining microvascular perfusion, the extent of myocardium at risk, and coronary flow reserve. The clinical utility of MCE is undergoing evaluation. The combination of DSE and MCE might provide an improved estimate of the extent of viable myocardium based on assessment of function and perfusion. Meanwhile, echocardiographic and nuclear techniques can be used to complement each other in the assessment of myocardial viability.