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。     

低剂量多巴酚丁胺负荷MR结合心肌标记技术在心肌缺血中的应用

目的评价采用心肌标记技术的低剂量多巴酚丁胺负荷MR用于检测缺血心肌室壁运动异常的价值。方法8只犬通过结扎左冠状动脉前降支第一对角支远侧建立急性心肌梗死模型后,行低剂量多巴酚丁胺负荷下的电影MR(c ine-MR)和采用心肌标记技术的低剂量多巴酚丁胺负荷下的c ine-MR,分析和对比左心室壁运动。结果c ine-MR扫描负荷前后的左心室各节段室壁运动得分指数(wallmotion score index,WMSI)有显著差异(1.44±0.16 vs 1.32±0.16,P=0.002),采用标记技术扫描负荷前后也有显著差异(1.48±0.12 vs 1.21±0.10,P=0.001)。而且,2种不同方法检测的负荷下的WMSI也有明显差异(1.32±0.16 vs 1.21±0.10,P=0.049)。结论采用心肌标记技术的低剂量多巴酚丁胺负荷下的c ine-MR比未采用心肌标记技术检测出更多的室壁运动异常,它是一种客观准确评价室壁运动异常的工具。     

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。     

慢性冬眠心肌动物模型的建立

 目的 建立理想的实验性猪慢性冬眠心肌动物模型.方法 体重8～10 kg幼猪开胸分离冠状动脉左前降支近段并置入C形缩窄环,饲养21周后行冠状动脉造影、99mTc-MIBI单光子发射型计算机断层心肌灌注显像、小剂量多巴酚丁胺负荷超声检查,最后取心肌组织行放射性微球测定心肌血流量、氯化-2,3,5-三苯基四氮唑检测梗死面积和透射电镜组织学检查.结果 冠状动脉造影显示左前降支近段完全或接近完全闭塞,闭塞端以远依靠侧枝循环供血.心肌灌注显示左前降支供血区心肌呈放射性稀疏.左前降支供血区域心肌符合已知的慢性冬眠心肌的病理生理学特征:静息状态下室壁增厚率明显下降[(8.2±3.2)% vs (41.3±6.3)%,P<0.01]并对多巴酚丁胺负荷呈明显双相反应,室壁平均心肌血流量和心内膜下心肌血流量显著降低[0.86±0.1 vs 1.05±0.06 ml/(min·g),P<0.05和0.71±0.06 vs 1.15±0.04 ml/(min·g),P<0.01],经检测未发现心肌坏死,透射电镜显示心内膜下心肌细胞肌小节减少,核周有大量小线粒体聚集,核内出现异染色质.结论 在幼猪冠脉左前降支近段置入C形缩窄环并饲养21周后,可成功建立慢性冬眠心肌动物模型,能为深入探讨冬眠心肌的病理机制提供实验基础.     

MRI评估心肌活性

心肌梗塞后心肌活性的诊断是为了评估血运重建后梗塞心肌功能恢复的可能性.MRI提供了多种评估心肌活性的方法.测量舒张期室壁厚度是一种易于操作的方法,这种方法敏感性高,但特异性低,只有在梗塞4个月后才能使用.低剂量多巴酚丁胺负荷实验对预测室壁运动的恢复情况有很好的敏感性和特异性,但其仅适用于单一节段的心肌功能障碍且心功能只有轻度下降的病人.延迟增强可直接显示坏死心肌和疤痕组织.通过判断坏死心肌延迟增强后的透壁程度,能够精确判断心肌舒缩能力恢复的可能性.首过灌注显示微血管阻塞,延迟增强能提供有关病人心肌活性及预后的信息.代谢成像技术,例如31P和23Na磁共振波谱可提供有关心肌梗死机制及活性方面进一步的信息.综述MRI评估心肌活性的方法和机制.     

多巴酚丁胺负荷试验对心肌纵向收缩功能的影响

目的 :联合使用多巴酚丁胺负荷试验与组织速度成像对局部纵向心肌的收缩功能进行定量分析 ,为临床诊断冠心病和评估存活心肌提供可靠的超声定量方法。方法 :对 18例冠状动脉造影正常或轻度病变和 61例冠心病心肌梗死心功能不全患者进行多巴酚丁胺负荷试验。对正常组和冠心病心肌梗死组基础状态 ,5、10和 2 0 μg/ (kg·min)所测的心肌收缩期峰速度进行统计学分析。结果 :冠脉造影正常组基础状态下 ,各室壁基底部收缩期峰值速度大于心尖部 ,而且呈现一定的规律 ,即基底部大于中部 ,中部又大于心尖部的速度梯度变化 ;侧壁 ,后壁和下壁收缩期峰值速度大于后间隔、前间隔和前壁。其中下、后壁心肌的峰值速度大于其它节段。多巴酚丁胺药物负荷时 ,心肌各节段收缩期峰值速度随着多巴酚丁胺剂量的增加而增加 ,2 0 μg/ (kg·min)收缩期峰值速度达最大值 ;40 μg/ (kg·min)时 ,收缩期峰值速度反而降低。在多巴酚丁胺药物负荷的不同阶段 ,仍然保持基础状态下的速度梯度规律和侧壁 ,后壁和下壁心肌收缩期峰值速度大于后间隔、前间隔和前壁心肌收缩期峰值速度的规律。 5 μg/ (kg·min)时 ,二维超声心动图显示各节段心肌运动无变化 ,但定量负荷显示其心肌收缩峰值速度已明显增加 ,且与基础状态比较差异有显著性意     

MRI评估心肌活性

心肌梗塞后心肌活性的诊断是为了评估血运重建后梗塞心肌功能恢复的可能性。MRI提供了多种评估心肌活性的方法。测量舒张期室壁厚度是一种易于操作的方法，这种方法敏感性高，但特异性低，只有在梗塞4个月后才能使用。低剂量多巴酚丁胺负荷实验对预测室壁运动的恢复情况有很好的敏感性和特异性，但其仅适用于单一节段的心肌功能障碍且心功能只有轻度下降的病人。延迟增强可直接显示坏死心肌和疤痕组织。通过判断坏死心肌延迟增强后的透壁程度，能够精确判断心肌舒缩能力恢复的可能性。首过灌注显示微血管阻塞，延迟增强能提供有关病人心肌活性及预后的信息。代谢成像技术，例如31^P和23^Na磁共振波谱可提供有关心肌梗死机制及活性方面进一步的信息。综述MRI评估心肌活性的方法和机制。     

小剂量多巴酚丁胺负荷试验对急性心肌梗塞早期心肌存活性的检测

目的 :探讨小剂量多巴酚丁胺负荷超声心动图 (LDDSE)检测急性心肌梗塞 (AMI)心肌存活的可靠性和安全性。材料和方法 :对 2 5例AMI后两周患者 ,在接受冠状动脉成形术治疗前后应用LDDSE检测 ,比较分析其室壁节段性运动异常的改变 ,以判断心肌存活性。结果 :在冠状动脉血运重建术前对室壁节段收缩功能的恢复预测准确率为 80 .2 % ,检测中并发症发生率极低 ( 4 % )。结论 :LDDSE对AMI早期可以较准确预测术后缺血心肌功能的恢复部位 ,安全性好。     

彩色室壁动力技术小剂量多巴酚丁胺负荷试验检测冬眠心肌与病理学检查对比的实验研究

目的: 探讨彩色室壁动力技术(CK)小剂量多巴酚丁胺超声心动图负荷试验(CK-DSE) 检测冬眠心肌(HM)的价值.材料和方法: 22只犬结扎冠状动脉造成实验性心肌缺血损伤的动物模型.应用CK-DSE检测动物模型的心肌梗塞区心内膜运动幅度/非梗塞区心内膜运动幅度比值(AMI/ANMI),与病理组织切片显示冬眠心肌面积/梗塞区总面积的比值(ATAM/ATIM)进行对比分析.结果: 本实验成功地建立11只实验性心肌缺血损伤的动物模型,CK-DSE检测冬眠心肌的敏感性、特异性和准确性分别为90%、80%和83%.CK-DSE检测AMI/ANMI比值,与ATAM/ATIM具有较好的相关关系(r=0.75).结论: CK-DSE能准确地检出心肌梗死后存活的冬眠心肌,是定量检测梗塞区内冬眠心肌的较好方法.     

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。     

Contrast enhancement for the myocardium.

The potential of MR imaging and spectroscopy in ischemic heart disease is substantial. MR contrast media have the potential to improve the differential tissue characterization among normal, ischemic, and infarcted myocardium. Several reports in animals and patients have revealed that MR contrast media can improve the delineation of acute myocardial infarctions (1–7). Studies from several centers in Europe and Asia have demonstrated that the contrast between the normal and acutely infarcted myocardium substantially increased with the use of gadolinium-DTPA administered intravenously (1, 2, 4, 5). In these studies, the acutely infarcted myocardium on delayed MR scans demonstrated greater enhancement with the paramagnetic contrast media than normal myocardium, producing a greater percentage contrast between the two regions. These studies are consistent with previous reports using gadolinium-DTPA contrast media to enhance the differential in signal intensity between the normal and infarcted myocardium in animal models (3, 6, 7). The expanded use of MR in ischemic heart disease will likely depend upon employing contrast media to enhance regional myocardial signal in proportion to regional blood flow. Such contrast media are needed for using MRI to demonstrate regions of myocardial ischemia and to depict reperfusion of a myocardial region after an ischemic event. © 1991 Academic Press, Inc.     

Blood pool contrast agent CMD-A2-Gd-DOTA-enhanced MR imaging of infarcted myocardium in pigs.

The purpose of this study was to assess the ability of the new blood pool contrast agent meglumine-carboxymethyldextran-ethylenediamino-gadoterate (CMD-A2-Gd-DOTA) to depict acute occlusive myocardial infarction (AMI). First-pass gradient-echo and delayed spin-echo magnetic resonance imaging (MRI) was performed 5 days after induction of AMI in a pig model. MRI was correlated with pathology. First-pass imaging with CMD-A2-Gd-DOTA allowed detection of infarcted myocardium in all pigs (n = 7). The infarction was recognized as a black spot on MRI as well as on a parametric image. The signal intensity (SI) amplitudes of normal versus infarcted myocardium were 80.55 +/- 18.61 versus 8.48 +/- 15.50 on MRI and 81.62 +/- 18.50 versus 1.61 +/- 3.73 on the parametric image (both P values < 0.001. The contrast ratio between normal and infarcted myocardium was not significantly improved on spin-echo MRI, suggesting largely intact vascular integrity outside the occluded area. CMD-A2-Gd-DOTA is useful for depicting occlusive myocardial infarction by first-pass MRI. Spin-echo imaging is promising in assessing vascular integrity. J. Magn. Reson. Imaging 1999;10:170-177.     

Myocardial blood flow at rest and contractile reserve in patients with chronic coronary artery disease and left ventricular dysfunction

BACKGROUND: The mechanisms that determine chronic left ventricular dysfunction in coronary artery disease (in particular, critical reductions in coronary artery blood flow leading to hibernating myocardium) may affect the ability of the myocardium to respond to inotropic stimulation with dobutamine. This study was designed to investigate the relationship between resting myocardial blood flow and contractile reserve in patients with coronary artery disease and chronic left ventricular dysfunction. METHODS AND RESULTS: Twenty-three patients (21 men and 2 women; age 61 +/- 9 years) underwent transesophageal echocardiography during infusion of dobutamine (2.5 microg/kg to 40 microg/kg per minute) and positron emission tomography (PET) with 150-water (9 patients) or 13N-ammonia (14 patients). Systolic wall thickening at each dose of dobutamine and resting myocardial blood flow were quantitatively analyzed in 8 anatomically matched regions at mid-ventricular level. Myocardial regions with preserved contraction had higher blood flow compared with regions with basal dyssynergy (0.99 +/- 0.3 vs 0.65 +/- 0.3 mL/min/gm; P < .0001). Among myocardial regions with preserved resting contraction, no relation was observed between blood flow and the response to dobutamine (r = 0.06). In contrast, among myocardial regions with diminished resting contraction, a significant correlation was observed between resting blood flow and contractile reserve (r = 0.53; P < .0001). The maximum increase in percent systolic wall thickening with dobutamine was 32.8% +/- 14% in regions with normal blood flow, 21.5% +/- 17% in regions with mildly to moderately reduced blood flow, and 10.7% +/- 10% in regions with severely reduced blood flow (P < .0001). CONCLUSIONS: These findings emphasize the importance of resting myocardial blood flow for the preservation of contractile reserve in patients with coronary artery disease and left ventricular dysfunction. Because a positive inotropic response to dobutamine is more likely to occur in dyssynergic regions with preserved rather than reduced myocardial blood flow, regional perfusion may determine in which circumstances dobutamine echocardiography contributes to the assessment of myocardial viability.     

Magnetic resonance imaging of chronic myocardial infarcts in man

To evaluate the magnetic resonance imaging (MRI) features of chronic myocardial infarction (MI), 22 patients and several normal volunteers were studied with a 0.35-T cryogenic imaging system. The MIs were 9 months to 16 years old. The patients also had either left ventriculography (17 patients) or two-dimensional echocardiography (17 patients). At least one abnormality indicative of prior infarction was demonstrated on MRI in 20 of the 22 patients. Wall thinning was seen in 20 patients; in six of these, the thinning resulted in aneurysm formation. The other 14 patients had sufficient residual wall thickness to permit measurement of T2 relaxation times and MR signal intensity in the infarcted region. Ten of these 14 patients demonstrated low intensity and shortened T2 of the thinned segments (mean T2 = 28.7 msec) compared to adjacent normal myocardium (mean T2 = 45.4 msec) and to the myocardium of volunteers (mean T2 = 41.3 msec). The percentage of difference in intensity between thinned and normal myocardium was greater on 56-msec-TE images (98.2%) than on 28-msec-TE images (46.1%). In the other four patients, no difference in intensity of the myocardium was perceptible in the thinned region of the myocardial wall. Thus MRI shows regional wall thinning at the site of prior MI. In some patients, the chronic infarct is characterized as decreased spin-echo signal intensity and shortened T2 consistent with replacement of myocardium by fibrous scar.     

Stunned,infarcted, and normal myocardium in dogs: simultaneous differentiation by using gadolinium-enhanced cine MR imaging with magnetization transfer contrast

PURPOSE: To simultaneously differentiate stunned, infarcted, and normal myocardial regions by using gadolinium-enhanced cine magnetic resonance (MR) imaging with magnetization transfer contrast. MATERIALS AND METHODS: Twelve dogs were imaged on days 1 and 8 after transient 90-minute coronary artery occlusion. A magnetization transfer contrast with echo-train readout (MTET) MR sequence was performed before and 30 minutes after gadolinium contrast enhancement. Ex vivo analysis consisted of MR imaging, microsphere blood flow analysis, and triphenyltetrazolium chloride (TTC) staining. A paired two-tailed t test was used to compare wall thickening from day 1 to day 8. Linear regression and Bland-Altman analyses were used to compare infarct size depicted with MTET imaging with that seen on TTC-stained tissue. RESULTS: Severe wall motion abnormalities were detected in all dogs. At TTC analysis, seven dogs had evidence of myocardial infarction and five had evidence of stunned myocardium. The mean percentages of left ventricular wall thickening in infarcted, stunned, and remote myocardial regions were 2% +/- 4 (SD), 4% +/- 8, and 33% +/- 5, respectively. Wall thickening did not improve in the infarcted zones, but it improved to nearly normal levels in the stunned region 1 week after induced occlusion (mean, 40% +/- 8; P <.02). MTET images clearly depicted infarcted myocardium as brighter than both the normal and stunned myocardial regions but darker than the blood pool. In vivo MTET infarct volume correlated with ex vivo TTC analysis data (y = 1.01x + 0.00, R = 0.98, standard error of the estimate = 0.019). CONCLUSION: One day after myocardial ischemia, MTET during one MR imaging examination enabled simultaneous differentiation of infarcted, stunned, and normal myocardial regions on the basis of gadolinium enhancement and regional function.     

Computed tomography of the normal and infarcted myocardium.

After intravenous administration of contrast agent, in vitro cardiac scanning showed a significant difference between the attenuation coefficients of the intracavitary blood pool and the myocardial wall, permitting clear delineation of the ventricular cavity. A substantial alteration in hematocrit permitted similar visualization of the intracavitary blood pool-myocardial wall interface. The attenuation coefficient of infarcted myocardium differed sufficiently from that of normal myocardium to render computed tomographic distinction feasible. In three hour old infarctions, the differences between normal and ischemic or infarcted tissue were enhanced by prior administration of contrast agent. These differences in attenuation coefficient indicate that a properly gated CT scanner could be utilized as a noninvasive approach to evaluating suspected or known myocardial infarction and other aspects of cardiac structure and function both in man and in experimental animals.     

Assessment of myocardial viability by MRI.

Assessment of myocardial viability has become an important issue in patients presenting with either acute myocardial infarction or presenting with chronic ischemic left ventricular dysfunction. In patients with viable myocardium recovery of left ventricular function can be anticipatedm, spontaneously in patients with acute myocardial infarction or following revascularization in patients with ischemic cardiomyopathy. In contrast, patients without viable tissue are not likely to improve in left ventricular function. Currently, nuclear imaging techniques and dobutamine stress echocardiography are used for assessment of viability; recent studies with magnetic resonance imaging (MRI) have however demonstrated the potential usefulness of this technique for the assessment of viability. Various parameters, derived from resting MRI, can be used as markers of myocardial viability, including the end-diastolic wall thickness, systolic wall thickening and signal intensity without contrast-enhancement. Other studies have combined the information from resting MRI with the assessment of contractile reserve during dobutamine stimulation. Finally, recent studies have evaluated the use of contrast-enhanced MRI to detect viable myocardium. All of these parameters are potentially useful and MRI provide an alternative approach for the assessment of viable myocardium.     

心脏节段性室壁厚度变化在冠心病MRI诊断中的价值

探讨节段室壁厚度变化在冠心病诊断中的价值。材料与方法：分析３１例冠心病和１１例正常对照组的ＭＲ电影,判断ＭＲ电影对冠心病的检测率。结果：正常对照组心肌各室壁厚度变化一致,缺血和梗塞心肌节段室 壁壁厚度变化明显小于正常心肌。     

Magnetic resonance imaging of ischemic heart disease

Magnetic resonance imaging (MRI) has several attributes important for evaluating ischemic heart disease. Internal cardiac anatomy is well delineated owing to inherent contrast between the blood pool and the cardiac walls. Using relaxation times and signal intensity differences, it is possible to discriminate between infarcted (acute and chronic) and normal myocardium. Gated MRI can also be used to quantitate regional myocardial infarction.