家猪急性心肌梗塞模型冠脉零流量压与存活心肌的相关性

目的:探索制备的家猪急性心肌梗塞模型中梗塞相关冠状动脉零流量压(Pzf)与存活心肌面积的关系。方法:普通家猪13只,冠脉造影结束后应用指引导管测量前降支近端压力,置入冠脉内多普勒导丝测量前降支远端冠脉内的血流速度,绘制压力-血流速度坐标轴,计算Pzf。将球囊送至冠状动脉左前降支中远端,堵闭血流60～100min,建立心梗模型。模型建立后重复测算前降支Pzf,分析心梗模型制备前后前降支Pzf数值的变化。处死试验动物,切片心肌采用TTC染色法识别梗塞心肌与存活心肌,采用图像分析仪分析代表存活心肌的颜色占整个左心室面积的百分数,将其与梗塞后前降支Pzf数值联合建立坐标轴,观察二者之间的关系。结果:所有家猪均完成冠状动脉左前降支远端的封堵,2只家猪分别在堵闭45和65min时因心室纤颤死亡。存活11只家猪均成功地建立急性心肌梗塞模型,完成Pzf数值的测算。心梗后前降支的Pzf[(53.06±23.01)mmHg]较心梗前[(40.13±19.53)mmHg]显著升高,P0.001。线性回归分析显示,TTc染色存活心肌占左心室面积的百分数与测得的Pzf值呈负相关(r=-0.879,P0.001)。结论:运用经皮腔内冠状动脉成形术球囊封堵冠状动脉可成功建立猪急性心肌梗塞模型,存活心肌的面积与相关血管的零血流量压呈负相关,提示零流量压的测定可以作为预测心梗后存活心肌范围的一个指标。     

冠状动脉堵闭法建立猪心肌梗死模型

探讨运用经皮腔内冠状动脉成形术球囊堵闭猪冠状动脉建立急性心肌梗死动物模型的实验方法。选用苏中幼猪11只，麻醉后经股动脉或颈总动脉置入经皮腔内冠状动脉成形术球囊至冠状动脉左前降支远端，堵闭血流120min。观察心电图、心肌酶、心脏二维超声检查及冠状动脉和左心室造影。结果发现，存活7只猪均完成冠状动脉左前降支远端的封堵，心电图显示急性心肌梗死典型图形变化，血浆肌钙蛋白明显升高并呈动态演变：术后1h超声检查出现间隔上部及前壁局部运动异常；术后2至4周造影复查显示左心室前壁、心尖部心室壁异常运动；存活7只猪均成功地建立急性心肌梗死模型。另4只猪分别在堵闭60～100min因心室纤颤死亡。结果提示，运用经皮腔内冠状动脉成形术球囊封堵冠状动脉可成功建立猪急性心肌梗死模型，并保持封堵冠状动脉通畅；与开胸法相比更接近人体状态，具有创伤小、动物生存时间长并易于术后馒头等优点。     

经皮球囊扩张封堵冠状动脉前降支制备巴马香猪急性心肌梗死模型

目的 探讨经皮球囊扩张封堵冠状动脉前降支(LAD)制备巴马香猪急性心肌梗死(AMI)模型的方法及可行性.方法 经右股动脉置入冠状动脉球囊导管至左前降支;预适应3～4次,每次球囊充盈30 s,间隔5～10 min;以3～5 atm扩张球囊封闭LAD远端血流,40 min后撤除球囊.结果 8头巴马香猪中有6头存活,造模成功率为75%.模型梗死面积变异系数为11.7%(33.2±3.9).封堵后心电图呈动态变化,心肌酶学指标(CK、CK-MB、cTnI、Myo、LDH)较术前明显升高,心脏彩超左心室舒张末内径、左心室舒张末容积及左心室收缩末容积均增大,LVEF均下降,部分实验猪出现心室壁瘤,TTC染色、HE染色证实心肌梗死模型建立成功.结论 经皮球囊扩张封堵法制备巴马香猪急性心肌梗死模型成功率高,保持了梗死区冠脉可重复进行造影,为干细胞植入梗死区心肌治疗AMI提供了较好的动物模型.     

球囊封堵法建立猪急性心肌梗死模型及MR判定

目的:运用球囊封堵法建立猪急性心肌梗死(AMI)模型,通过磁共振(MR)判定模型建成与否。方法:实验使用12头小型猪,麻醉后经右侧股动脉将球囊导管置入至左前降支第1对角支下方0.5~1.0 cm处堵闭90 min,直至心电图证实AMI形成,并行MR True Fisp-PSIR序列心肌延迟灌注扫描及HE染色。结果:12头小型猪中10头成功建立AMI模型,MR延迟灌注扫描在T1WI双反转序列上,室间隔呈半月形低信号。HE染色法显示,封堵血管远端的心肌细胞核淡染、胞浆溶解。结论:冠状动脉球囊堵法是一种简单安全的建立AMI模型的方法,MR可更直观地观察到梗死区面积、组织水肿及心功能改变。     

非开胸法建立室壁瘤动物模型的实验研究

目的　探讨运用PTCA球囊封堵猪冠状动脉建立急性心肌梗死后室壁瘤的动物模型的实验方法。方法　选用家猪 7只 ,麻醉后经颈总动脉或股动脉置入PTCA球囊至左前降支 (LAD)第一对角支远端 ,对堵血流 15 0分钟。观察 :心电图、心肌酶、心脏二维超声检查及冠状动脉和左心室造影。结果　 7只猪均完成LAD的封堵 ,2只分别在堵闭 12 0分钟和 2 0分钟后因心室纤颤死亡。存活的 5只猪成功建立左室前壁急性心肌梗死模型 ,术后 6周造影复查示左室前壁、心尖部室壁瘤形成 ,4只猪堵闭的LAD远端闭塞。心电图显示急性心肌梗死的典型图形和动态演变过程。cTnI明显升高并呈动态演变。术后 1小时超声检查出现间隔上部及前壁局部运动异常 ,术后 2周即有室壁瘤形成。结论　运用PTCA球囊封堵冠状动脉可成功建立急性心肌梗死后室壁瘤的动物模型 ,与开胸法相比更接近人体的状态 ,具有创伤小、动物成活率高、生存时间长、技术要求不高等优点 ,可为进一步的研究提供较好的实验模型。     

经皮穿刺心外膜电-解剖标测及射频消融心肌梗死后室性心动过速的实验研究

目的探讨经心外膜途径在电-解剖标测系统指导下行射频消融治疗心肌梗死后室性心动过速的可行性和安全性。方法成年中华小型猪共7只,采用经皮穿刺的方法将球囊置于左前降支中下部,封堵150 min建立心肌梗死模型。3～5周后将心肌梗死模型猪,行电生理检查诱发室性心动过速。经胸穿刺进入心包腔,采用电-解剖标测系统在窦性心律下进行心外膜电压标测和线性消融。射频消融后再次行电生理检查,不能再诱发室性心动过速为消融成功。结果存活的心肌梗死模型的猪7只,3～5周后行电生理检查,共诱发出单形性室性心动过速共8种,7种表现为右束支阻滞图形,1种表现为左束支阻滞图形,室性心动过速(VT)周长平均在(338±66)ms。1只猪同时诱发心室颤动,电除颤转复窦性心律。7只猪心包穿刺均成功,完成心外膜电压标测,沿瘢痕区到二尖瓣环或正常心肌区逐点进行线性消融。射频消融后再次行电生理检查,6只猪不能再诱发室性心动过速。结论经胸穿刺进入心包腔行心外膜标测和消融治疗心肌梗死后室速的方法是安全可行的,心外膜标测消融心肌梗死后室速的方法可以作为心内膜消融的一种有效补充方法。     

多巴酚丁胺负荷试验结合斑点追踪成像技术识别心肌梗死犬存活心肌的实验研究

目的:应用多巴酚丁胺负荷试验,结合斑点追踪成像(STI)技术,识别心肌梗死犬危险区的存活心肌。方法:于实验犬左冠状动脉(冠脉)前降支分出第1对角支后约1cm处结扎,建立心肌梗死犬模型。结扎3h后行多巴酚丁胺负荷试验,剂量组分别为0、5、10、20、30和40μg·kg-1·min-1,每个剂量组持续推注3min,分别采集心尖四腔、心尖两腔、心尖三腔切面图像。负荷试验结束后处死犬,游离心脏,行Evans Blue和TTC双染色。STI定量分析0μg·kg-1·min-1时危险区梗死心肌的节段数,同时结合心肌染色结果计算其中的存活心肌节段数,然后分析负荷试验不同剂量组条件下的心肌运动,判断其识别存活心肌的准确率。结果:120只犬成功建立心肌梗死模型。结扎3h后,0μg·kg-1·min-1时STI定量分析梗死心肌节段数61个,Evans Blue和TTC双染色显示其中的存活心肌节段数42个,其收缩期长轴应变率峰值(SrLP)为(0.48±0.24);40μg·kg-1·min-1条件下STI识别出存活心肌节段数39/42个,准确率92.9%,其SrLP明显改善(-0.65±0.45),与0μg·kg-1·min-1相比,差异有统计学意义(P0.01)。结论:多巴酚丁胺负荷试验结合STI技术能准确识别危险区的存活心肌。     

介入技术建立心肌梗死猪动物模型

目的:建立基于介入技术的猪心肌梗死模型。方法:家猪18只,34月龄,体质量5065 kg,戊巴比妥钠麻醉后以球囊导管推送海绵颗粒至冠状动脉左前降支远端,造成冠状动脉左前降支远端闭塞。结果:17只猪成功建立心肌梗死模型,1只死亡。10只存活时间大于3个月,6只术后8周按计划处死,1只术后第二天处死,无意外死亡。结论:以球囊导管推送海绵颗粒栓塞冠状动脉建立猪心肌梗死模型,方法简便易行,动物可长期存活。     

急性心肌梗死后心脏结构和神经重构的实验研究

目的探讨家猪急性心肌梗死(简称心梗)后心脏结构和神经重构的相关分子机制。方法 16只家猪在禁食12h,禁饮4h后随机分为假手术组(n=6)和心梗组(n=10)。应用置入经皮冠状动脉腔内球囊堵闭前降支的方法制备家猪心梗模型(假手术组放置球囊,但不堵闭);利用超声心动图观察心梗后心脏结构特性,三维标测系统检测左室电压改变。同时应用免疫组化、Western blot和ELISA实验方法分析心肌结构及神经重构相关因子的含量变化。结果心梗组4只家猪因心室颤动死亡。与假手术组比较,心梗组舒张期室间隔厚度和左室舒张期后壁厚度均变薄(P<0.05),而左室舒张末期内经变大(P<0.05);左室短轴缩短率和左室射血分数变小(P<0.05)。与假手术组比较,心梗组神经生长因子相关蛋白-43、酪氨酸羟化酶标记的阳性神经密度明显增加(P<0.05),神经抑制因子Sema3a表达明显下降(P<0.05);心梗组白介素-1β、肿瘤坏死因子-α、内皮素-1、神经生长因子、促血管生成素-2表达明显上调(P<0.05)。结论急性心梗后心脏结构和神经重构发生重大改变,此将影响心肌的功能特性。     

尼沙赫电图对早期心肌缺血的预先诊断价值探讨

目的 建立中国中型猪经皮冠状动脉腔内血管成形术(PTCA)球囊封堵冠状动脉急性心肌梗死模型,研究急性心肌缺血梗死过程中尼沙赫电图(saahECG)时间轴心室测量标量参数S-VS和VS-VD的变化,并探讨该变化对心肌缺血的早期诊断价值.方法 中国中型猪,体重39~67(44.5±12.70)kg,麻醉后经股动脉置入PTCA球囊至左前降支第一对角支远端,堵闭血流120 min,同步、逐波扫描记录模型建立前后及过程中saahECG和常规12导联心电图(ECG),随后对saahECG时间轴心室测量,以S-VS和VS-VD作为标量参数进行分析,并与同步记录的ECG对比分析.结果 ①运用PTCA球囊封堵法成功建立猪急性心肌梗死模型,球囊封堵12 s后saahECG即出现VS-VD改变,39 s后S-VS显著增加,而ECG的ST段改变则于24 s后出现.②saahECG心室时间轴标量参数S-VS、VS-VD改变早于心电图改变.③ 球囊封堵前及封堵2 h后,saahECG标量参数S-VS、VS-VD差异显著.结论 我们发现了一种新的监测心肌缺血的体表心电图,即saahECG,saahECG比ECG提前反应,并可以实现心肌缺血改变的数据化显示,对心肌缺血更早期的诊断有重要价值.     

Correlation between electrical and mechanical properties of the left ventricle in patients with postinfarction ventricular tachycardia

BACKGROUND: Electroanatomical mapping allows differentiation between viable and scarred myocardium. Echocardiography is widely used to assess myocardial contractility. The relationship between electrophysiological and echocardiographic assessment of left ventricular function has not yet been well established. AIM: To correlate mechanical and electrical function of the left ventricle in patients with postinfarction ventricular tachycardia and to assess clinical, echocardiographic and angiographic parameters affecting regional electrical function. METHODS: In 32 patients (25 males, 64+/-9 years old) mean unipolar (UP) and bipolar (BP) voltages were obtained with electroanatomical mapping (CARTO system) for a 12-segment model and compared with segmental wall motion function scored as normal, hypokinetic and a- or dyskinetic. UP voltage in individual groups of segments was: 7.8+/-4.2 mV, 6.5+/-4.2 mV, 4.7+/-2.5 mV, p <0.01 and for BP voltage 2.1+/-1.5 mV, 1.9+/-1.9 mV, 1.1+/-1.0 mV, p < 0.01, respectively. Left ventricular ejection fraction < or =30%, end-diastolic diameter >56 mm, previous inferior or anterior myocardial infarction (MI), MI < or =5 years and open infarct-related artery were associated with lower voltage in normokinetic segments. CONCLUSIONS: Segments with advanced systolic dysfunction had significantly lower uni- and bipolar voltage than normo- and hypokinetic segments. However, preserved local electrical function could be found in a/dyskinetic regions. Left ventricular remodelling, time and location of MI and patency of infarct-related artery influenced voltage in normokinetic segments.     

药物负荷三维超声心动图检测存活心肌的价值

目的：利用药物负荷三维超声心动图试验,检测心肌梗死患者的存活心肌。方法：50例心肌梗死患者行冠脉血液灌注重建术（PCI,CABG）,在术前行三维超声心动图检查和多巴酚丁胺负荷超声试验,根据术后一个月复查心脏超声结果左室整体EF较术前改善〉5％与否分为存活心肌组（41例）和无存活心肌组（9例）,三维超声检查时进行左室三维重建,将左心室分为17个节段,比较负荷试验前后左室整体射血分数（EF）及左室壁各节段的射血分数EF值。结果：术后1月多巴酚丁胺负荷三维超声试验：与负荷试验前比较,存活心肌组于负荷试验时左室整体EF值[（40±13）％比（53±15）％,P〈0．05],梗死区相关节段EF值[（33±12）％比（50±18）％,P〈0．01]均明显改善;无存活心肌组负荷试验前后左室整体EF值,梗死区相关节段EF值无明显改善（P均〉0．05）。心梗患者于冠脉术后1月复查三维超声心动图,存活心肌组左室整体EF值术前、术后为（40±13）％,（49±15）％,改善20％,无存活心肌组EF值术前、术后为（36±8）％,（38±10）％,改善≤5％。结论：多巴酚丁胺负荷三维超声心动图检查对心肌梗死患者存活心肌的检测客观、可定量,有一定的临床应用价值。     

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.     

经静脉心肌声学造影评价心肌梗死后存活心肌的价值

目的　探讨经静脉心肌声学造影 (MCE)对心肌梗死后存活心肌的诊断价值。方法　 2 4例心肌梗死患者用二维超声评价室壁运动情况 ,同时经静脉进行MCE ,以 3个月后静态超声心动图左室心肌节段性运动改善为依据评价MCE对心肌梗死后存活心肌的诊断价值。结果　在 2 4例病人的 384个心肌节段中 ,运动异常节段 184个。在运动异常的 184个节段中 ,MCE1分 39段 ,0 5分 5 0段 ,0分 95段。 3个月复查 79个节段有运动改善 ,其中 39段来自MCE1分的心肌 ,4 0段来自MCE0 5分的心肌。MCE对预测心肌梗死后室壁运动改善的敏感性、特异性、阳性预测值、阴性预测值及准确率分别为 :10 0 %、89 7%、84 8%、10 0 %和 94 6 %。结论　MCE能比较准确地预测心肌梗死后心肌的存活性     

Endocardial electromechanical mapping in a porcine acute infarct and reperfusion model evaluating the extent of myocardial ischemia

OBJECTIVE: Catheter-based, left ventricular, electromechanical mapping (EMM) has evolved as a diagnostic tool to characterize ischemic and injured myocardium. In the acute setting, diagnostic criteria for ischemic or infarcted myocardium are not well defined. In the present study, the capacity of separating myocardium with evolving necrosis from viable myocardium was investigated. METHODS AND RESULTS: Pigs were subjected to balloon occlusion of the left anterior descending coronary artery for 45 minutes. Using the NOGATM cardiac mapping system, EMM was performed at the baseline and after two hours of reperfusion. EMMs were evaluated regarding unipolar voltage (UPV), bipolar voltage (BPV) and local linear shortening (LLS). The pigs were sacrificed four hours after reperfusion and morphological estimation of infarct size and localization was performed. Baseline UPV activity was significantly lower in the anterior, lateral and posterior basal segments as compared to the septal and posterior midventricular segments. After reperfusion, UPV, but not BPV, was significantly decreased in the apical, midventricular septal and basal segments. LLS demonstrated significant impairment of mobility in the septal midventricular segment. The thresholds for separating electromechanical activity at baseline from after infarction differed between the myocardial regions. The ability of EMM to correctly detect infarcted myocardium showed a sensitivity and specificity in the order of 50 85%, as compared to the morphological standard. CONCLUSION: In a porcine acute infarct and reperfusion model, electromechanical activity thresholds, for infarct detection, could be established, but there was significant intersegmental threshold variability at baseline and after infarction. Accordingly, applying general thresholds demonstrated a poor correlation between infarct extension evaluated by EMM and morphology.     

Validation of viability assessment by electromechanical mapping by three-dimensional reconstruction with dobutamine stress echocardiography in patients with coronary artery disease

We evaluated the ability of electromechanical mapping (EMM) to discriminate between normal, viable, and nonviable (scarred) myocardium in patients with coronary artery disease versus dobutamine stress echocardiography (DSE) when the correspondence between the test and reference data sets is established via a common 3-dimensional reconstruction of the left ventricle. We studied 21 patients with coronary artery disease who underwent angiography, biplane ventriculography, and EMM within 1 month of DSE. A 3-dimensional left ventricular (LV) reconstruction was prepared from the ventriculogram and spatially aligned with EMM. EMM measurements of unipolar voltage, bipolar voltage, and local linear shortening were projected onto the three-dimensional left ventricle, averaged in each of 16 segments, and compared with DSE viability (normal, viable, scar) assessed at a core laboratory. All of the EMM measurements varied significantly (p <0.001) between the normal, viable, and scarred myocardium as assessed by DSE. Local linear shortening for normal, viable, and scarred segments was 10.4 +/- 6.5%, 7.8 +/- 5.6%, and 4.8 +/- 4.4%, respectively. In discriminating between these 3 groups, local linear shortening was more powerful than unipolar voltage or bipolar voltage (F = 20.765, F = 10.655, F = 4.795, respectively). Local linear shortening correlated best with viability, perhaps because it shares the same cognitive function as DSE. Three-dimensional analysis provides an anatomic framework that enables direct comparison of data from multiple imaging modalities rather than assuming segmental correspondence. Our results show that EMM provides significant on-line, diagnostic information on myocardial viability assessed by DSE on a segment-by-segment basis.     

Relationship between successful ablation sites and the scar border zone defined by substrate mapping for ventricular tachycardia post-myocardial infarction

INTRODUCTION: It is unknown if identification of scar border zones by electroanatomical mapping correlates with successful ablation sites determined from mapping during ventricular tachycardia (VT) post-myocardial infarction (MI). We sought to assess the relationship between successful ablation sites of hemodynamically stable post-MI VTs determined by mapping during VT with the scar border zone defined in sinus rhythm. METHODS AND RESULTS: Forty-six patients presenting with hemodynamically stable, mappable monomorphic VT post-MI and who had at least one such VT successfully ablated were prospectively included in the study. In each patient, VT was ablated by targeting regions during VT that exhibited early activation, +/- isolated mid-diastolic potentials, and concealed entrainment suggesting a critical isthmus site. Prior to ablation, a detailed sinus-rhythm CARTO voltage map of the left ventricle was obtained. A voltage <0.5 mV defined dense scar. Successful VT ablation sites were registered on the sinus voltage map to assess their relationship to the scar border zone. Of the 86 VTs, 68% were successfully ablated at sites in the endocardial border zone. The remaining VTs had ablation sites within the scar in (18%), in normal myocardium (4%), and on the epicardial surface (10%). There were no significant differences in VT recurrence amongst the different groups. CONCLUSION: Successful ablation sites of hemodynamically stable, monomorphic VTs post-MI are often located in the scar border zone as defined by substrate voltage mapping. However, in a sizable minority, ablation sites are located within endocardial scar, epicardially, and even in normal myocardium.     

Electromechanical mapping for detecting myocardial viability and ischemia in patients with severe ischemic cardiomyopathy

This study was designed to evaluate several electromechanical mapping parameters for assessment of myocardial viability and inducible ischemia as defined by dipyridamole single-photon emission computed tomographic (SPECT) imaging at rest in patients with severe ischemic cardiomyopathy. Unipolar voltage, normalized unipolar voltage, bipolar voltage, and fragmentation were compared with tracer uptake at rest and reversibility on stress or rest quantitative technetium-99m sestamibi SPECT imaging in 32 patients with severe ischemic cardiomyopathy (left ventricular ejection fraction 0.24 +/- 0.08). In dysfunctional myocardial segments, logistic regression showed unipolar voltage, normalized unipolar voltage, and bipolar voltage to be predictive of viable myocardium (> or = 60% tracer uptake at rest) and was significantly higher in viable than in nonviable segments (p <0.01). A unipolar voltage of > or = 7.1 mV was the best predictor of viable myocardium. In dysfunctional viable segments, unipolar voltage was significantly higher in reversible than in fixed segments (p <0.001), and a unipolar voltage of > or = 8.5 mV had optimal power for identifying reversibility on dipyridamole SPECT imaging. We conclude that in patients with severe ischemic cardiomyopathy, unipolar voltage can identify viable from nonviable myocardium and reversible from fixed viable defects as defined by dipyridamole technetium-99m sestamibi SPECT imaging.     

二维应变成像结合腺苷负荷超声心动图评价犬存活心肌

目的 探讨二维应变成像结合腺苷负荷超声心动图评价存活心肌的新方法.方法 15只健康杂种犬,结扎其冠状动脉前降支90 min后,恢复血流灌注120 min,建立急性心肌梗死再灌注模型.分别于基础状态下(结扎前)和再灌注后采集心尖三腔、两腔和短轴二尖瓣、乳头肌、心尖水平的图像.随后泵入腺苷并重复采集图像.以氯化三苯基四氮唑溶液(2,3,5-triphenyl tetrazolium chloride,TTC)染色结果测量梗死面积(SN)与该节段总面积(S)的百分比(SN/S),SN/S≤50%即为存活心肌.将前壁、前间壁各节段分为存活心肌和非存活心肌,运用二维应变成像技术定量评价犬不同状态下存活与非存活心肌径向、纵向及圆周的收缩期峰值应变(peak-systolic strain,Speak sys)并进行比较.结果 存活与非存活心肌分别为37和53个节段.(1)基础状态下:存活与非存活心肌的收缩期峰值径向应变(RSpeak sys)、纵向应变(LSpeak sys)及圆周应变(CSpeak sys)比较差异无统计学意义.(2)再灌注120 min后:存活与非存活心肌的RSpeak sys、LSpeak sys及CSpeak sys(绝对值)均低于基础状态,而存活心肌与非存活心肌组间差异无统计学意义.(3)腺肾负荷后:与再灌注120 min后相比,存活心肌的RSpeak sys、LSpeak sys显著升高(P<0.01或P<0.05),且存活心肌的RSpeak sys、LSpeak sys明显高于非存活心肌(P<0.01).(4)腺苷负荷后,RSpeak sys与SN/S呈负相关(r=-0.72,P<0.01),CSpeak sys及LSpeak sys与SN/S呈正相关(r值分别为0.40和0.67,P均<0.01).(5)将腺苷负荷前、后应变数值的变化率(△RSpeak sys和△LSpeak sys)作为研究对象,以△RSpeak sys≥13.5%作为判断心肌存活的最佳截断值,其识别存活心肌的敏感性和特异性分别为83.8%、83.0%;以△LSpeak sys≥11%作为最佳截断值,其敏感性和特异性分别为78.4%、88.7%;联合△RSpeak sys和△LSpeak sys两项指标,其敏感性和特异性分别为91.9%、79.2%.结论 二维应变成像技术结合腺苷负荷超声心动图能比较准确地区分存活心肌与非存活心肌.