中华小型猪急性心肌缺血的综合影像学研究

目的 研究MSCT、MRI、SPECT对中华小型试验猪急性心肌缺血模型的显示效果.方法 中华小型猪共6只,所有试验猪接受MSCT扫描1次后结扎前降支中远段,在结扎后2、4、6、8 h内,每2 h MSGT扫描1次.术后24 h内进行MR、SPECT及再次完成MSCT扫描各1次,最后处死动物行病理检查.使用重复测量因素的方差分析,比较左心室前壁首过灌注减低区域与左心室侧壁首过灌注无减低区域的首过灌注CT值从术前至术后2、4、6、8、24 h的变化;使用单因素方差分析检验术前及术后2、4、6、8、24 h的心功能变化;使用配对t检验分析比较氯化三苯基四氮唑(TTC)染色病理、MSCT、MRI相互间测量梗死面积的百分比.结果 术中死亡动物1只,完成检查5只.术后2、4、6、8及24 h的MSCT动脉期减低区域,术后24 h SPECT显示的灌注减低区域,MRI显示的首过灌注减低区,病理显示的心肌梗死大致范围均位于左心室前壁.3只试验猪4～8 h的MSCT延迟扫描出现灌注减低区域边缘强化.动脉期灌注减低区域的术前与术后各时间段的CT值分别为75.9、36.4、35.2、37.8、37.4、33.3 HU,差异均有统计学意义(F=12.341,P＜0.01),术后各时间段间的CT值差异没有统计学意义(F=2.278,P=0.792).术前及术后2、4、6、8、24 h的每搏输出量(SV)平均容积分别为21.7、11.9、10.3、11.4、12.3、12.6 ml(F=22.349,P＜0.01);收缩末期(ESV)平均容积分别为15.2、23.4、25.0、24.4、25.3、22.8ml(F=8.810,P＜0.01);舒张末期(EDV)平均容积分别为37.0、35.4、35.0、35.7、37.6、37.5 ml(F=2.339,P=0.079);射血分数(EF)平均依次为58.9%、33.8%、29.0%、31.9%、32.6%、33.5%(F=27.240,P＜0.01),除EDV外差异均有统计学意义.5只猪测得的梗死面积占所测层面整个心肌比例分别为MSCT(39.4±12.6)%、MRI(37.2±10.0)%,TTC(35.9±9.6)%.TTC与MSCT(t=0.612,P=0.574)、TTC与MRI(t=0.820,P=0.458)、MSCT与MRI(t=0.425,P=0.692)间差异均无统计学意义.结论 MSCT动脉期、MRI首过灌注、SPECT显示梗死区域与TTC染色梗死部位均位于左心室前壁.MSCT动脉期与MRI首过灌注显示的低灌注面积与TTC染色梗死面积有很好的相关性.急性心肌缺血后24 h内缺血心肌密度、心功能没有随时间发生变化.     

中华小型猪心肌微循环障碍的影像学研究

目的：MSCT、MRI和SPECT对中华小型猪心肌微循环障碍的显示效果。方法：中华小型猪8只,全部雄性,体重（22．8±0．9）kg。实验猪接受MSCT扫描1次后1周内于前降支中远段注射105直径约100um微球,术后27天行SPECT,28天行造影、MSCT和MRI检查各1次,最后处死动物送病理检查。结果：4只实验猪死亡,其余4只完成所有检查。病理染色未均见梗死。术前与术后28天MSCT扫描测量每搏输出量、收缩末期容积、舒张末期容积和射血分数的差异均无统计学意义（P〉0．05）。术前与术后28天的MSCT扫描测量左室前壁、左室侧壁及室间隔的平均CT值在动脉期、延迟1、3、5和10min自身对照均没有统计学差异。术后28天的左室前壁、左室侧壁及室间隔在MSCT动脉期均未见异常灌注减低区域,延迟扫描也未出现强化;MRI均未见异常灌注减低区域,延迟扫描也未见强化;SPECT扫描示上述区域均未见明显灌注减低区域。结论：MSCT、MRI和SPECT对于没有明显病理染色的梗死区域及心功能变化的微循环障碍显示是受限的。     

急性心肌缺血再灌注的MRI与定量病理对照研究

目的 研究心肌急性缺血再灌注损伤的MRI特征及其病理学基础。材料与方法 阻断家兔冠状动脉左前降支40min再灌注1h后行MR平扫，Gd-DTPA动态增强，电影MRI（cine-MRI)及多巴酚丁胺负荷试验，放射微球测定心肌血流，伊文氏蓝和TTC染色确定正常，危险和梗死心肌行病理和体视学测量。结果 危险和梗死心肌强度曲线与正常表现不同，静息cine-MRI均显示损伤区运动减弱，室壁变薄，心脏射血分数减低，多巴酚丁胺负荷后则运动增强，室壁增厚，心脏射血分数增加。结论 急性缺血再灌注损伤后，不同的损伤区具有不同的定量病理学特征；Gd-DTPA动态增强,cine-MRI及多巴酚丁胺负荷试验可以提高对心肌急性缺血再灌注损伤检出的敏感性和准确性，预测心肌活性。     

超声、磁共振对冬眠心肌及其存活性的实验研究

目的:探讨超声和MR评价冬眠心肌及其存活性的价值。材料和方法:通过Ameroid环套扎猪冠脉的左回旋支完成6个冬眠心肌模型,分别于术前、术后2、5周进行超声和MR检查。结果:超声显示左室侧后壁运动异常区,在5、10μg/(kg.min)多巴酚丁胺刺激下,室壁运动改善,在20μg/(kg.min)多巴酚丁胺刺激下,有2头猪室壁运动恶化。MR显示2头猪有心内膜下梗死,与病理结果一致,判断的坏死心肌范围术后5周较2周时缩小;有1头猪病理显示缺血而MR灌注成像未见缺血节段。结论:多巴酚丁胺负荷超声及MR灌注成像可以识别冬眠心肌,MRI延迟显像高信号可能高估坏死心肌。     

犬急性心肌梗死磁共振心肌灌注及电影成像实验研究

目的　采用MR快速序列研究急性心肌梗死的首过灌注特点及心功能改变。材料与方法　犬心肌梗死模型 9只 ,均进行T1WI磁化准备梯度回波序列 (TurboFLASH)首过灌注扫描及MR电影成像 (cine MR) ,完成检查后处死 ,分析心肌首过灌注特点及局部心功能变化 ,并与病理检查比较。结果　首过灌注时梗死心肌表现为灌注缺损 ,信号强度 时间曲线上升延缓 ,曲线斜率和峰值信号强度分别为 0 .0 2 5± 0 .0 2 0和 0 .84± 0 .2 7,较正常心肌(0 .13± 0 .0 80和 2 .0 2± 0 .99,P <0 .0 0 0 1)明显下降 ,峰值时间和曲线上升时间分别为 37.78± 11.90s和 32 .70±14 .0 9s,较正常心肌 (17.14± 6 .0 6s和 14 .2 8± 5 .14s,P <0 .0 0 0 1)明显延长。延迟期正常心肌信号强度下降 ,而梗死心肌仍呈上升趋势。首过灌注中灌注缺损面积与TTC染色一致。梗死节段室壁运动及室壁厚度异常。结论　MR首过灌注成像可反映病变心肌组织血流灌注信息 ,cine MR能测定节段室壁功能。结合首过灌注和心功能分析 ,可对梗死心肌在形态学和功能学两方面进行定性、定量分析 ,有助于评价梗死心肌活力     

猪急性心肌梗死模型cTnI与DE-MRI相关性实验研究

目的探讨临床试剂盒是否适用于猪心肌梗死模型心肌肌钙蛋白(cTnI)的检测,其检测的cTnI峰值与DE-MRI所检测心肌梗死积分的关系。材料与方法 10只制备成功的猪急性心肌梗死模型分别于术前、术后1h、2h、5h、24h、48h、72h、1周采血行cTnI检测,所用试剂盒为临床试剂盒;术后行延迟增强MRI(DE-MRI)检查,心脏标本行氯化三苯基四氮唑(TTC)染色和免疫组织化学检查。结果 10例TTC染色和免疫组织化学均证实有心肌梗死;10例cTnI术后1h可见上升,于24h达高峰,24h峰值与DE-MRI、TTC检测的心肌梗死积分高度相关,相关系数分别为0.84、0.855(P值<0.05),有显著统计学意义。结论临床试剂盒对猪血清cTnI术前及术后检测,可反映猪心肌损伤;其24h峰值与DE-MRI心肌梗死范围强相关;两者均可活体内检测,且对坏死心肌有高度敏感性,两者结合有助于结果的相互印证和互为补充,可更准确地评价心肌梗死。     

Gd-DTPA动态增强MRI评价心肌微血管损伤

目的：探讨Gd-DTPA动态增强MRI评价心肌微血管损伤的可行性。方法：制作急性犬心肌梗死动物模型，在活体上用放射微球^99Tc—MAA测量心肌血流量，0．5％伊文蓝染色区分缺血心肌；心脏离体后用3％TTC染色区分梗死心肌，SP免疫组化染色观察心肌微血管并计算微血管体积分数。犬离体心脏左冠状动脉插管后作MRI平扫及Gd—DTPA动态增强扫描，测量正常、缺血和梗死心肌的信号强度，绘制时间-信号强度曲线。结果：在T1WI上，心肌信号强度无明显差异；在T2WI上，病变心肌信号强度较正常增高；Gd-DTPA灌注动态增强扫描，正常心肌时间-信号强度曲线呈下降形，危险心肌呈上升形，梗死心肌呈平直形，灌注晚期病变区呈明显环状强化。正常、危险和梗死心肌血流量、微血管体密度差异显著。结论：急性心肌梗死后心肌间质水肿、心肌含水量增加致T2WI信号增高。Gd-DTPA动态增强时间-信号强度曲线上升的斜率及峰值可以反映心肌微血管损伤及组织水肿的程度。     

磁共振心肌灌注成像急性心肌梗死的实验研究

目的 研究猪急性心肌梗死的首过灌注和延迟时相MRI特点.方法 猪心肌梗死模型12只,均进行快速梯度回波序列(FGREET)首过灌注扫描及反转恢复梯度回波序列(MDE)延迟时相扫描.扫描后处死,分析心肌首过灌注和延迟时相特点,并与病理检查对照.结果 9例(75%)首过灌注时梗死心肌表现为灌注减低,其信号强度显著低于周围心肌,10例(83.33%)延迟期梗死心肌表现为延迟强化,而正常心肌信号强度下降,低于梗死心肌.结论 MR心肌灌注成像可有效检测急性心肌梗死的梗死心肌以及其程度和范围.     

磁共振多技术联合应用检测存活心肌的实验研究

目的　评估磁共振多技术联合应用检测心肌存活的价值。材料与方法　选择慢性心肌缺血模型猪 2 0只 ,分别于制作模型前、后 1～ 2个月行磁共振多技术联合应用扫描 (形态、电影扫描、心肌灌注和心肌活性扫描 ) ,判断心肌缺血区和坏死区的大小 ,并与病理结果对照了解其准确性。结果　MRI检查发现 2 0只猪中有 3只形态扫描见左室侧壁变薄 ;负荷电影扫描见 11(11/2 0 )只猪左心室收缩功能正常 ,有 9(9/2 0 )只静息时左室节段不同程度运动减弱 (n =7)或丧失 (n =2 )。多巴酚丁胺负荷电影扫描检测到 7只猪左室节段功能改善 ,但有 2只猪无明显改善。心肌灌注扫描有 13只猪共 4 7.8个节段缺血 ,心肌活性扫描有 8只猪共 2 3.6个节段坏死 ,病理检查发现共有 7只猪 2 3个节段坏死。与MRI延迟强化区所显示的梗死区一致 ,差异无统计学意义 (t=0 .0 4 5 ,P >0 .0 5 )。结论　磁共振多技术联合应用可有效检出缺血、坏死心肌 ,并准确判断其程度和范围     

急性心肌梗塞的MRI特征及其超微病理基础

目的　探讨急性心肌梗塞后不同心肌损伤区的MRI特征及其超微病理学基础。方法　结扎兔冠状动脉左前降支 2 4h制作AMI模型 10只 ,行常规MRI、对比剂动态增强MRI、电影MRI及多巴酚丁胺负荷试验。放射微球测定心肌血流量 ,伊文氏蓝和TTC染色确定缺血和梗塞心肌 ,并制作电镜标本观察肌原纤维和线粒体的改变 ,测定病变值和对损伤程度分级。结果　AMI后T1信号无明显改变 ,T2 信号增高 ,40 %可见病变局部心肌壁变薄 ,60 %可见病变邻近左室腔内异常血流高信号 ;正常、缺血和梗塞心肌动态增强时间 -信号强度曲线表现不同 ;cine -MRI表现为局部室壁变薄、运动减弱 ,多巴酚丁胺负荷表现为室壁变厚、运动增强。病变心肌较正常肌含水量显著增高而血流显著减少。正常、缺血及梗塞心肌线粒体体密度、数密度存在显著差异。结论　AMI的MRI表现与心肌超微结构损伤程度及残余血流量有关     

Myocardial adrenergic derangement due to myocardial ischemia: decreased myocardial uptake of I-123 metaiodobenzylguanidine after PTCA in a patient with effort angina

Regional denervation of adrenergic nerves has been clinically demonstrated in patients with myocardial infarction using I-123 metaiodobenzylguanidine (MIBG) scintigraphy. However, it is not clarified whether adrenergic denervation can be induced by prolonged myocardial ischemia as well as by myocardial infarction. This case with effort angina had 99% stenosis of right coronary artery and showed perfusion defects at inferior myocardial regions in the exercise thallium-201 study. However, inferior wall motion estimated by echocardiography and left ventriculography was normal indicating the absence of myocardial infarction. After percutaneous transluminal coronary angioplasty for the stenosis, I-123 metaiodobenzylguanidine (MIBG) and thallium-201 (Tl-201) myocardial scintigraphies were done to estimate the therapeutic effect of PTCA. Although the Tl-201 study during exercise showed normal findings indicating the success of PTCA, marked defects was detected at inferior myocardial regions in the I-123 MIBG studies just after and 4 hours after an intravenous injection of I-123 MIBG. These results suggest that adrenergic derangement may be induced by prolonged myocardial ischemia and may persist for periods even though myocardial perfusion is normalized.     

The Significance of Perfusion Defect at Myocardial Perfusion MR Imaging in a Cat Model of Acute Reperfused Myocardial Infarction

Objective

To determine whether the size of a perfusion defect seen at myocardial perfusion MR imaging represents the extent of irreversibly damaged myocardium in acute reperfused myocardial infarction.

Materials and Methods

In nine cats, reperfused myocardial infarction was induced by occlusion of the left anterior descending coronary artery for 90 minutes and subsequent reperfusion for 90 minutes. At single-slice myocardial perfusion MR imaging at the midventricular level using a turbo-FLASH sequence, 60 short-axis images were sequentially obtained with every heart beat after bolus injection of gadomer-17. The size of the perfusion defect was measured and compared with both the corresponding unstained area seen at triphenyl tetrazolium chloride (TTC) staining and the hyperenhanced area seen at gadophrin-2-enhanced MR imaging performed in the same cat six hours after myocardial perfusion MR imaging.

Results

The sizes of perfusion defects seen at gadomer-17-enhanced perfusion MR imaging, unstained areas at TTC staining, and hyperenhanced areas at gadophrin-2-enhanced MR imaging were 20.4 ± 4.3%, 29.0 ± 9.7%, and 30.7 ± 10.6% of the left ventricular myocardium, respectively. The perfusion defects seen at myocardial perfusion MR imaging were significantly smaller than the unstained areas at TTC staining and hyperenhanced areas at gadophrin-2-enhanced MR imaging (p < .01). The sizes of both the perfusion defect at myocardial perfusion MR imaging and the hyperenhanced area at gadophrin-2-enhanced MR imaging correlated well with the sizes of unstained areas at TTC staining (r = .64, p = .062 and r = .70, p = .035, respectively).

Conclusion

In this cat model, the perfusion defect revealed by myocardial perfusion MR imaging underestimated the true size of acute reperfused myocardial infarction. The defect may represent a more severely damaged area of infarction and probably has prognostic significance.     

Detection of regional myocardial perfusion deficit using rest and stress perfusion MRI: a feasibility study

OBJECTIVE: Providing high temporal and spatial resolution, perfusion MRI is an attractive alternative to traditional radionuclide methods like SPECT and PET. Although first-pass perfusion MRI examinations have gained increasing attention during the past years, this technique still exhibits relatively low signal-to-noise ratio and cardiac coverage. Previous studies have suggested that refocused gradient sequence technology (e.g., true fast imaging with steady-state precession [FISP]) should improve perfusion MRI examinations. The aim of this study was to assess myocardial perfusion deficits in patients with proven coronary artery disease using a saturation recovery true FISP perfusion sequence. SUBJECTS AND METHODS: Rest and stress perfusion MRI studies were performed in 22 patients with coronary artery disease at 1.5 T using a multislice saturation recovery true FISP sequence after the bolus injection of 0.025 mmol/kg of body weight of gadopentetate dimeglumine. The myocardium of each slice was divided into 12 radial segments with subdivision into subendocardial and subepicardial subregions. Myocardial perfusion was assessed semiquantitatively and independently for each subregion. The standard of reference for myocardial perfusion was SPECT. Delayed enhancement images were acquired after the injection of 0.15 mmol/kg of body weight of gadopentetate dimeglumine. RESULTS: Sensitivity and specificity of perfusion MRI examinations for the detection of perfusion deficits were 81% and 89%, respectively, for the semiquantitative perfusion parameter upslope and 78% and 86% for the parameter peak signal intensity. More specifically, rest perfusion examinations were able to detect areas of infarction, whereas stress examinations increased the perfusion differences between normal and ischemic myocardial areas. Excellent correlation was observed between rest perfusion and late enhancement findings (r = 0.90). CONCLUSION: In patients with single-vessel coronary artery disease, perfusion deficits can reliably be detected using a saturation recovery true FISP sequence. Semiquantitative perfusion parameters upslope and peak signal intensity yielded similar results.     

MRI for the evaluation of regional myocardial perfusion in an experimental animal model

Myocardial perfusion was assessed in nine pigs using ultrafast gradient-echo MRI (.5 T, 15-mT/m gradients) at different levels of myocardial blood flow (range, .005–1.84 ml/min/g), generated either by adenosine infusion or by a mechanical occluder, and measured independently using radiolabeled microspheres. Sixty-four consecutive, ECG-triggered, diastolic, short axis images of the left ventricle were obtained during intravenous bolus injections (y = 30) of .05 mmol/kg of gadopentetate dimeglumine. Relative changes in peak intensity, time to peak intensity, washin slope, correlation coefficient, and cross-correlation coefficient were computed from the time-intensity curves obtained from four regions of interest, namely septal, anterior, lateral, and inferior walls. The values from the inferior wall acted as reference for evaluating relative changes in the other three regions. The cross-correlation coefficient (P < .001, r = 60) and the peak intensity (P < .001, r = .72) showed the best correlation with myocardial blood flow. The washin slope showed a weak positive trend (P < .05), but the low value of r (r = .28) indicated that the use of this parameter to predict flow was invalid; the correlation coefficient and time to peak intensity were not correlated ( P = ns). In conclusion, this study shows that it is possible to evaluate relative myocardial perfusion after the first pass of a an intravenously injected bolus of gadopentetate dimeglumine, using dynamic MRI on a conventional medium field MRI system. The cross-correlation coefficient and the peak intensity resulted in more efficient parameters to evaluate relative inhom-ogeneity of regional myocardial perfusion.     

MRI detection of myocardial perfusion defects due to coronary artery stenosis with MS-325

PURPOSE: To assess the value of an intravascular, albumin-targeted contrast agent, MS-325, in visualizing myocardial ischemia with magnetic resonance imaging (MRI). MATERIALS and METHODS: Left anterior descending coronary artery (LAD) stenosis was created in 19 pigs using a closed-chest modified angioplasty technique. Myocardial ischemia was detected by first-pass, contrast-enhanced MRI at peak dipyridamole stress and was compared to Technetium-99m (Tc-99m) sestamibi single photon emission computed tomography (SPECT). Regional coronary blood flow was determined using microspheres. RESULTS: Inducible myocardial ischemia with >40% reduction in stress myocardial blood flow was created in eight animals. An MRI defect, classified as > or=75% reduction in peak myocardial signal intensity in the affected territory, was detected in 92.3% of these animals. In the presence of mild coronary stenosis, there was uniform enhancement with MRI and tracer uptake by SPECT. Concordance of MRI and SPECT for detecting perfusion defects was 85%. CONCLUSION: The pattern of prolonged and persistent MR hypoenhancement of the ischemic myocardial bed using MS-325, which is retained primarily in the vascular bed due to its albumin-binding properties, facilitates the detection of myocardial perfusion defects.     

A method to remove artifacts in attenuation-corrected myocardial perfusion SPECT Introduced by misalignment between emission scan and CT-derived attenuation maps.

Nonuniform soft-tissue attenuation affects the diagnostic accuracy of SPECT in myocardial perfusion imaging. The attenuation map required for attenuation correction can be acquired using x-ray tomography (CT). Frequent findings in attenuation-corrected images are defects in the apical and anterior myocardial wall. We assume that these are artifacts produced by misalignment of SPECT images and the attenuation map. METHODS: One hundred forty patients underwent myocardial perfusion imaging with 99mTc-methoxyisobutylisonitrile. Twenty-seven of 140 showed pronounced defects in the apical or anterior wall only after CT-based attenuation correction. SPECT and corresponding CT slices were examined for misalignment in the ventrodorsal direction (y-direction) visually and by threshold-based delineation of the body surface. Mismatched studies were realigned and image reconstruction and analysis were redone. The effect of the correction was assessed visually and by semiquantitative analysis based on a 20-segment model using 4D-MSPECT. RESULTS: In 15 of 27 patients, the improved coregistration led to smaller and less-pronounced defects in the regions mentioned. In 6 of 27 patients, former defects were judged as normal. No improvement was seen in only 4 patients. In these 4 subjects, the mismatch in the y-direction was <1 pixel (7 mm), and visual inspection suggested a coincident mismatch in the craniocaudal direction. In 2 cases, coregistration was not possible because the body outline extended beyond the CT field of view. Semiquantitative analysis revealed a significant increase of the relative uptake in the apex; in the apical segments of the anterior, septal, and inferior wall; and in the mid-anterior and mid-anteroseptal segment. Basal segments of the anterolateral, lateral, and inferolateral wall and the middle inferolateral segment showed a significant decrease of relative uptake. CONCLUSION: Misalignment in the y-direction between SPECT and the attenuation map can lead to artifacts in the apical, septal, and anterior wall, which will appear as defects. It also can cause overcorrection in the basal inferior and lateral segments. There is evidence that mismatches along the other directions may have a similar effect. The coregistration of SPECT and the attenuation map needs to be verified for every patient, even when using integrated dual-modality imaging devices.     

MR imaging evaluation of myocardial viability in the setting of equivocal SPECT results with (99m)Tc sestamibi

PURPOSE: To determine if contrast material-enhanced magnetic resonance (MR) imaging is useful for assessment of myocardial viability in patients with equivocal stress-rest results from single photon emission computed tomographic (SPECT) examination with technetium 99m sestamibi. MATERIALS AND METHODS: Twenty patients underwent stress-rest SPECT examinations with sestamibi. Results were considered equivocal for assessment of myocardial infarct on the basis of fixed perfusion defects that either had normal wall motion or exceeded any wall motion abnormalities. Patients then underwent (a). contrast-enhanced MR imaging for assessment of myocardial infarct and (b). cine MR imaging for assessment of wall motion. For image analyses, the left ventricle was divided into 14 segments. Wall motion and extent of infarct were assessed independently and compared. RESULTS: Forty-one segments were equivocal for infarct at SPECT, and most (21 of 41 [51%]) involved the posterior or inferior wall. Infarct was confirmed with MR imaging in 10 of 41 (24%) equivocal segments in eight patients (40%). An additional 29 segments in eight patients had infarct at MR imaging that was not suspected at SPECT, including segments in three patients with no clinical history of myocardial infarct prior to imaging. All cases of infarct except one that were equivocal or undetected with sestamibi at SPECT were nontransmural at MR imaging, and most of the unsuspected subendocardial infarcts (15 of 28 [54%]) had no associated wall motion abnormalities. CONCLUSION: Patients with radionuclide examination findings that are equivocal for infarct may benefit from contrast-enhanced MR imaging, particularly in the setting of nontransmural infarct.